High-Fat or High-Carbohydrate Meal—Does It Affect the Metabolism of Men with Excess Body Weight?
by
, , ,
Lucyna Ostrowska
1
,
Joanna Smarkusz-Zarzecka
1,*,
Anna Muszyńska
1,
Edyta Adamska-Patruno
2,
Maria Górska
3 and
Adam Krętowski
3 1
Department of Dietetics and Clinical Nutrition, Medical University of Bialystok, ul. Mieszka I 4B, 15-054 Bialystok, Poland
2
Clinical Research Support Centre, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24a, 15-276 Bialystok, Poland
3
Department of Endocrinology, Diabetology and Internal Medicine, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24a, 15-276 Bialystok, Poland
*
Author to whom correspondence should be addressed.
Nutrients 2022, 14(14), 2876; https://doi.org/10.3390/nu14142876
Submission received: 8 June 2022
/
Revised: 8 July 2022
/
Accepted: 11 July 2022
/
Published: 13 July 2022
(This article belongs to the Section Nutrition and Metabolism)
Abstract
:Excessive adipose tissue in the body may lead to adverse health effects, carbohydrate and lipid metabolism disorders, and cardiovascular diseases. The aim of this study was to analyze the effect of a standardized high-fat meal (HF) on changes in energy expenditure and changes in the oxidation of energy substrates as well as the concentration of glucose, insulin, triglycerides and homocysteine in blood serum in relation to a standardized high-carbohydrate (non-fat, HC) meal in men with different nutritional status. In this study, 26 men (aged 19–60) without carbohydrate disorders (study group GS = 13 overweight/obese; control group GC = 13 normal body weight) were examined. It was observed that following a high-fat or high-carbohydrate meal, men with excessive body weight metabolized the main nutrients differently than men with normal body weight, and postprandial insulin secretion was also different (even without any significant differences in glucose concentrations). Overweight/obesity, which is in itself a risk factor for cardiovascular disease, contributes to an increase in the concentration of other risk factors, such as the concentration of homocysteine and triglycerides, which is referred to as cardiometabolic risk. Consumption of a high-fat meal increased the number of potential risk factors for cardiovascular disease (homocysteine and triglycerides) compared to a high-carbohydrate meal.
1. Introduction
Obesity has become a global problem. According to the latest data from the World Health Organization (WHO), the prevalence of obesity in the world almost tripled between 1975 and 2016. In 2016, over 1.9 billion adults had excess body weight, and 650 million of them were obese [1]. Obesity has been defined as a chronic disease with no tendency to resolve spontaneously and with a tendency to relapse [2]. Excessive accumulation of adipose tissue in the body, which exceeds physiological needs and adaptation abilities, can lead to adverse health effects, including carbohydrate and lipid metabolism disorders and cardiovascular disease (CVD) [3]. A new parameter in the assessment of carbohydrate and lipid homeostasis is postprandial dysmetabolism. Conventional risk factors for CVD are assessed in the fasting state. Postprandial dysmetabolism, however, is the postprandial state characterized by abnormally elevated levels of serum glucose and lipids, and is an independent risk factor for cardiovascular events [4]. Considering that most people eat fat-containing meals frequently during the day, the usual metabolism of lipids is postprandial since after fatty meal consumption, serum triglycerides increase within 1 h and remain elevated for 5–8 h. This contrasts with glucose metabolism, which displays transient elevation after a meal [5]. Elevated serum triglyceride and homocysteine levels are among the several risk factors for CVD [6]. In the treatment of obesity, pharmacological and non-pharmacological strategies are used. Caloric restriction and increased physical activity play a significant role in the non-pharmacological management of the disease. In clinical conditions, among the methods used to assess the effect of meals with different macronutrient content on energy expenditure and the oxidation of energy substrates is indirect calorimetry and the assessment of blood serum parameters. The method is based on the premise that the energy used by the body is obtained from the oxidation of nutrients (carbohydrates, proteins and fats) [7].
The broader focus of our research efforts is to evaluate potential differences in energy expenditure, glucose and lipid oxidation between men with different nutritional status and the impact of these variations on the further course of this disease in individuals with obesity [8]. Moreover, the limited number of scientific reports concerning the influence of the different nutritional composition of meals on energy expenditure and oxidation of nutritional substrates in the available literature encourages research in this area.
The aim of our study was to compare the effect of a standardized high-fat meal versus a standardized high-carbohydrate (non-fat) meal on changes in energy expenditure and the oxidation of energy substrates as well as the concentration of glucose, insulin, triglycerides and homocysteine in the blood serum of men with different nutritional status. We investigated the postprandial effect since direct and proportional associations between postprandial dysmetabolism and type 2 diabetes as well as cardiovascular diseases and events have been demonstrated [9,10].
2. Materials and Methods
This study was approved by the local Bioethics Committee of the Medical University of Bialystok, Poland (No. R-I-002/35/2009). This study is part of a larger project registered at clinicaltrials.gov as NCT03792685. In the present study, data from 26 individuals who met the inclusion criteria were analyzed. Inclusion criteria were: age 19–60 years and no carbohydrate metabolism disorders (to exclude people with carbohydrate disorders, a 75 g oral glucose tolerance test was performed). Exclusion criteria were: endocrine disorders, gastrointestinal diseases, renal/hepatic insufficiency, and other conditions that might have affected the final results, i.e., past bariatric and gastroenterological surgery, significant changes in body weight in the three months preceding this study, pharmacological treatment and use of other preparations, the influence of which on hormonal and metabolic changes in the body has not been documented or is not known. Only men were included in this study since the investigated parameters might have been characterized by sexual dimorphism, and therefore more confounding factors would have had to be considered in the analysis, such as hormones and menstrual cycle phases, which was not the aim of our study [11,12,13]. Men with a body mass index (BMI) ≥ 25.0 kg/m2 were included in the study group—GS (overweight/obese; n = 13). Men with a BMI < 25.0 kg/m2 were included in the control group—GC (normal body weight; n = 13). Participant characteristics are presented in Table 1.
Standardized, isocaloric meals with different nutritional composition were used to conduct the crossover study. The first was a high-fat (HF) meal (Calogen, Nutricia, Poland, 96% energy from fats, 4% from carbohydrates and 0% from proteins; energy value—−450 kcal) and the second was a high-carbohydrate (HC) meal (Nutridrink Fat Free, Nutricia, Poland, 89% energy from carbohydrates, 0% from fats and 11% from proteins; energy value −450 kcal). In order to obtain the energy value of both meals at the level of 450 kcal, a 300 mL portion of the HC meal and a 95 mL portion of the HF meal were used. Table 2 shows the composition of the HC and HF meals.
This study was conducted in two stages (two test meal visits). Subjects received the standardized HC or HF meals in random order, in a crossover design. Subjects arrived at our laboratory fasted between 6 and 10 a.m., and were asked to rest for 30 min in the supine position. Following that, cannulation of the antecubital vein was performed, and blood was collected for the determination of fasting glucose, insulin, triglyceride and homocysteine levels, and resting metabolism, fat and carbohydrate oxidation were assessed (30-min recordings). Then, the participants received a randomly assigned HC or HF meal (at room temperature) with a recommendation to consume it within 10 min. The subjects remained supine throughout the examination. Venous blood was drawn at 30, 60, 120, 180 and 240 min after HF or HC meal consumption to determine the concentration of glucose, insulin, triglycerides and homocysteine, while at 60, 120, 180 and 240 min after meal ingestion, energy expenditure was determined and glucose/lipid oxidation was assessed.
After 2 weeks, all participants received the second meal—HC or HF meal (those who had an HF meal during the first visit received an HC meal, and those who had ac HC meal on the first visit received an HF meal at room temperature)—and went through the same procedures as on the first visit.
2.1. Biochemical Analysis
The biochemical parameters were assessed at the Laboratory of the Department of Endocrinology, Diabetology and Internal Diseases, Medical University of Bialystok, Poland. Some of the parameters (glucose and triglycerides) were determined immediately after venous blood collection. The remainder of the biological material was stored in accordance with the recommendations of the manufacturers of the laboratory kits (−20 °C/−80 °C), and determinations were performed after the entire group of men had been tested. Serum glucose levels were measured by the hexokinase/glucose-6-phosphate dehydrogenase (G6PD) method using the Cobas c111 analyzer (Roche Diagnostics Ltd., Rotkreuz ZG, Switzerland). Serum insulin levels were assessed by the immunoradiometric method (RIA) with the use of INS-IRMA kits (DiaSource Immuno-Assays S.A., Ottignies-Louvain-la-Neuve, Belgium). The Wallac Wizard 1470 Automatic Gamma Counter (PerkinElmer, Life Science, Turku, Finland) was used for the determination of insulin. Serum triglycerides levels were determined by the enzymatic-colorimetric method according to Wahlefeld using the Cobas c111 analyzer (Roche Diagnostics Ltd., Rotkreuz ZG, Switzerland). Serum homocysteine levels were measured using the enzyme immunoassay (ELISA) method with the Human Homocysteine (Hcy) ELISA KIT (MyBioSource, Inc., San Diego, CA, USA).
2.2. Calorimetry Measurements
The assessment of resting metabolism, energy expenditure, the oxidation of fat and carbohydrates was conducted using the indirect calorimetry method with a metabolic monitor (Vmax Encore 29n System, Viasys HealthCare, Yorba Linda, CA, USA). All measurements during the indirect calorimetry test were performed with the participants lying down, in thermal comfort (room temperature within 21–25 °C), in a relaxed state, but with a recommendation not to fall asleep. Duration of a single recording of the test was approximately 30 min.
2.3. Statistical Analysi
Descriptive statistics were prepared by designating mean and standard deviation values for quantitative features. The studied group was taken as the classifying variable, and two levels of the classifying variable were determined: overweight/obese men (Gs) and normal body weight men (Gc). The choice of the statistical test depended on checking the following conditions: (1) homogeneity of variance in the groups and (2) normality of distribution of the dependent variable in the groups. If both conditions were met, one-way repeated-measures ANOVA was used, if not, the non-parametric Mann–Whitney U test was used. The area under the curve (AUC) of the values of the variables was calculated using the trapezoidal rule. The interrelationship between selected variables was obtained using the Spearman rank-order correlation coefficient (r). Statistical significance was set at p < 0.05. STATISTICA 13.3 (by Stat Soft, Cracow, Poland) was used for statistical analysis.
3. Results
In order to assess the effect of the investigated meals on the metabolic parameters in men with different nutritional status (without glucose disturbances), changes over the four-hour period in blood serum glucose, insulin, triglyceride and homocysteine concentrations following HF and HC meal ingestion were assessed, and the results are presented in Table 3.
3.1. Blood Glucose Concentration
Serum glucose concentrations and the AUC of serum glucose concentrations following the HF and the HC meal were very similar in men from both groups (Table 3, and Supplementary Figure S1a,b). Glucose AUC values were, as expected, statistically significantly higher after the HC vs. the HF meal both in GS (p = 0.0014) and GC (p = 0.0018) groups (Figure 1).
There were no statistically significantly correlations between postprandial serum glucose concentrations, following either the HF or the HC meal, and BMI.
3.2. Serum Insulin Concentration
Despite the absence of carbohydrate metabolism disorders in the Gs group of men, fasting serum insulin concentrations were higher in this group (Table 3) compared to subjects from the control group. After the HF meal, serum insulin concentrations in the GS group were significantly higher during the 30–180 min postprandial period compared to the control group (Table 3, Supplementary Figure S2a), which led to a significantly higher AUC of postprandial insulin concentrations in the GS group compared to the control group (Table 3, Figure 2).
Surprisingly, no statistically significant differences in serum insulin concentrations were found between studied groups during the four-hour observation period following HC meal consumption, although higher, but not statistically significant, postprandial insulin levels were observed after HC meal ingestion at 30, 60 and 120 min in the GS group (Table 3, Supplementary Figure S2b). However, as expected, the AUC of postprandial serum insulin concentrations was significantly higher following the HC vs. the HF meal, both in the GS (p = 0.0014) and GC (p = 0.0014) groups (Figure 2).
It was found that BMI was positively correlated with fasting insulin concentration (p = 0.0375; r = 0.4099). Statistically significant positive correlations were also observed between BMI and serum insulin concentration after HF meal ingestion at 120 (p = 0.0007; r = 0.6205) and 240 (p = 0.0386; r = 0.0386) minutes of the test. There were no significant correlations between serum insulin concentrations and BMI in either group after HC meal consumption.
3.3. Triglyceride Concentrations
We observed that fasting triglyceride concentrations as well as concentrations after the HF meal (at 30, 120, 180 min of test) and the HC meal (30–180 min of the test) were significantly higher in the GS group compared to the GC group (Table 3, Supplementary Figure S3a,b). The high serum triglyceride concentrations observed in the GS group were sustained for four hours after HF meal consumption, and resulted in higher AUC (GS: 39,867 mg/dL vs. GC: 26,685 mg/dL (p = 0.0240)), as shown in Figure 3. A statistically significantly higher AUC of triglyceride concentrations was also demonstrated in the GS group vs. the GC group after HC meal ingestion (p = 0.0274). Moreover, as we expected, significantly higher AUC values of triglycerides were observed in both groups: GS (p = 0.0159) and GC (p = 0.0071), following HF meal consumption in comparison to HC meal ingestion (Figure 3). Furthermore, a statistically significant positive correlation was demonstrated between BMI and the fasting serum concentration of triglycerides (p = 0.0142; r = 0.4749), and the concentrations at 120 (p = 0.0048; r = 0.5254) and 240 (p = 0.0427; r = 0.4002) minutes after the ingestion of the HC meal, which was not observed after HF meal consumption.
3.4. Homocysteine Concentrations
Statistically significantly (p = 0.0221) higher fasting homocysteine concentrations were found in the GS group in comparison to the GC group before HC meal ingestion. Higher serum homocysteine concentrations were also observed in the GS group after consumption of both HF and HC meals (Table 3, Supplementary Figure S4a,b). A statistically significant difference (p = 0.0040) was found in the AUC of serum homocysteine postprandial concentrations following the HF meal between the groups. Furthermore, statistically significant differences (p = 0.0138) were observed in the AUC of postprandial homocysteine concentrations after the HC meal between the GS and the GC groups (Table 3, Figure 4).
There were statistically significant positive correlations between BMI and serum homocysteine concentrations following both the HC meal (fasting: p = 0.001; r = 0.6690 and during the second hour of the test p = 0.0010; r = 0.6069) and the HF meal (in the second: p = 0.0012; r = 0.5970 and fourth hour of the test p = 0.0054; r = 0.5286)
3.5. Indirect Calorimetry
In both studied groups, changes in energy expenditure, carbohydrate and fat oxidation after the HF meal, and then after the HC meal were assessed, as shown in Table 4. There were no statistically significant differences between the groups in energy expenditure, and glucose and fat oxidation, both in a fasted state and after the HF meal. However, after the HC meal, a statistically significant higher glucose oxidation level was demonstrated at 240 min after the ingestion of the meal in the Gs group.
3.5.1. Energy Expenditure
There were no statistically significant differences between the groups in energy expenditure both in a fasted state, and following HF and HC meal ingestion (Table 4, Supplementary Figure S5a,b). A statistically significant difference (p = 0.0014) was found in the AUC of energy expenditure after the HC meal vs. the HF meal in the GS group (Figure 5).
3.5.2. Glucose Oxidation
We did not observe any significant differences between the groups in glucose oxidation, except for higher glucose oxidation in the Gs group at 240 min after the ingestion of the HC meal (p = 0.0479) (Table 4, Supplementary Figure S6a,b).
In the GC group, the AUC of glucose oxidation after the HC meal was significantly higher than after the HF meal (p = 0.0464), which was not observed in the GS group (Figure 6).
3.5.3. Lipid Oxidation
Higher levels of fasting lipid oxidation were observed in the GS group compared to the GC group (Table 4, Supplementary Figure S7a,b). A significantly higher AUC of lipid oxidation was observed in both the GS (p = 0.0014) and GC (p = 0.0392) groups after HF vs. HC meal ingestion (Figure 7).
4. Discussion
Treatment of obesity can be based on non-pharmacological methods and supportive treatment with the use of pharmacotherapy. Lifestyle modification, which involves altering long-term habits of eating and physical activity, and maintaing the new behaviour allows for a gradual and long-term reduction in body weight, and in particular a reduction in adipose tissue mass. Recently, monotrophic, unbalanced diets have become popular, and are considered the best methods of rapid weight loss. Scientific research indicates that long-term consumption of a high-fat diet has a negative effect on cardiometabolic risk. High-fat intake accompanied by restricted carbohydrate intake leads to changes in the hormonal balance, including low insulin concentration in the blood serum [14], which is also confirmed by our own research. Moreover, not only diets, but also single meals can induce significant adverse effects, called postprandial dysmetabolism, which is a postprandial state characterized by abnormal metabolism of glucose and lipids. Bell DSH. et al. demonstrated direct and proportional associations between postprandial dysmetabolism and increased inflammation, endothelial dysfunction, coronary artery disease as well as cardiac events [9]. There is evidence that postprandial dysmetabolism is associated with non-alcoholic fatty liver disease (NAFLD), increased cardiovascular mortality and morbidity, and some other diseases, mostly due to macro- and microvascular complications [15].
The current study demonstrated that a high-fat meal exerts an adverse effect on cardiometabolic risk factors (in particular, triglyceride and homocysteine concentrations), especially in overweight/obese individuals. Other authors have also observed an increase in serum triglyceride concentrations following a high-fat meal [16,17]. Furthermore, high-fat diets can significantly increase homocysteine concentrations, and thus have a detrimental effect on the function of the endothelium of blood vessels, particularly in people with excess body weight. Apart from affecting the lipid profile, impairment of endothelial function may be a possible mechanism in the pathophysiology of atherosclerosis from HF intake [18,19]. A study by Wycherley et al. also showed an increase in fasting homocysteine concentrations in individuals with excess body weight following consumption of a high-fat diet for one year [19]. However, not all studies have proven the effect of high-fat meals on homocysteine concentrations. In a study involving healthy adults, De Rose et al. did not find significant changes in serum homocysteine levels after HC or HF meal ingestion [20,21]. In the majority of scientific publications, high-protein diets were also the focus of interest in the context of the effect on homocysteine concentration [22].
Some authors suggest that changes observed in lipid levels depend on the duration of the diet. In the first six months, the changes may seem insignificant, while after a longer period, consumption of a high-fat diet may result in disturbances in lipid metabolism, mainly in the form of elevated levels of total cholesterol, triglycerides and serum homocysteine, thus increasing the risk of CVD. Changes in lipid concentrations seem to be particularly dangerous for people with obesity and dyslipidemia [20,21,22].
In the present study, postprandial serum glucose concentrations (followig HF and HC meals) were not statistically significantly correlated with BMI, which suggests that both overweight/obese and normal body weight individuals without carbohydrate metabolism disorders metabolize glucose similarly after HF and HC meal ingestion.
Our study demonstrated that consumption of a HF meal increased the number of potential risk factors for CVD (homocysteine and triglycerides) compared to a HC meal. Our research found that overweight/obesity, which is in itself a risk factor for CVD, contributes to an increase in the levels of other risk factors, such as the concentration of homocysteine and triglycerides [23]. We noted that in the 4 h postprandial period, glucose and insulin concentrations were significantly higher following the HC meal in comparison to the HF meal. Our study revealed that in overweight/obese men, a different metabolic response is evoked by the ingestion of both an HF meal and an HC meal in comparison to people with a healthy body weight consuming the same meals. It has been demonstrated that individuals with overweight/obesity, but without metabolic disorders, differ in their metabolic response to stimulation with dietary fat [21,24].
Analysis of the results obtained from indirect calorimetry measurements shows that the rates of energy substrate oxidation did not differ between the studied groups, except at 240 min following the HC meal, when higher glucose oxidation rates in subjects with overweight/obesity were noted. Comparable glucose oxidation following the consumption of both test meals observed in overweight/obese men may suggest the onset of metabolic flexibility disturbances. Resting metabolism and diet-induced thermogenesis were not significantly different between the studied groups. In the group of overweight/obese men, the HC meal caused higher energy expenditure, which may suggest that long-term consumption of a high-fat diet may result in weight gain due to its lower thermal effect.
The conclusions of our study encourage an extended follow-up of the body’s response to stimulation with different meals in order to better understand the long-term effects of different diets on cardiometabolic risk factors, especially because some scientific reports do not show any harmful effects of the long-term consumption of high-fat and low-carbohydrate diets on the cardiovascular system [25]. However, episodes of hypoglycemia after meals with a very high-carbohydrate content may significantly worsen metabolic control and increase the risk of developing cardiovascular diseases. Our study included men without carbohydrate metabolism disorders, but differences in the metabolic and hormonal responses following the ingestion of the test meals were observed between the men with normal body weight and those with overweight/obesity. Excess body weight may increase the risk of developing metabolic diseases, such as type 2 diabetes, dyslipidemia, atherosclerosis and metabolic syndrome. Hypertrophic adipocytes are also characterized by increased secretion of pro-inflammatory cytokines, which are considered potential risk factors for cardiovascular disease. Future research should focus on assessing the use of various monotrophic diets, and also traditional, unbalanced diets (in different populations of patients),and their impact on individual cardiovascular risk factors. Moreover, future research should also take into account nutrigenetic polymorphisms, which may also determine how the body metabolizes fats, proteins and carbohydrates.
We observed that following HF or HC meal ingestion, overweight/obese men metabolized the main nutrients differently than men with normal body weight, and postprandial insulin secretion was also different (even without any significant differences in glucose concentrations). Moreover, consumption of a HF meal increased the concentration of triglycerides and homocysteine in the blood serum. Both HF and HC diets may increase the risk of CVD, and therefore monotrophic diets should be avoided.
An important limitation of our study is a small sample size. The main reason for this was long observation time during the visits, which was approximately 7–8 h at a time. Another limitation of our study is assignment of eligible individuals to the groups only on the basis of their BMI index. An additional limitation of this study is assessment of only triglyceride concentrations in the blood serum of the participants, without taking into account the other parameters of lipid metabolism. Futher research in groups broken down by sex and age range, and the percentage of adipose tissue with an extension to the full lipid profile of the participants should be designed.
The value of this study is increased by the fact that the same subjects participated in the crossover study, and that it was based on standardized meals with the same energy value. Conducting further observations on a larger population is required and may lead to interesting conclusions that may be applicable in everyday clinical practice.
5. Conclusions
- It was observed that following a high-fat or high-carbohydrate meal, men with excessive body weight metabolize the main nutrients differently than men with normal body weight, and postprandial insulin secretion is also different (even without any significant differences in glucose concentrations).
- Overweight/obesity, which is in itself a risk factor for cardiovascular disease, contributes to an increase in the concentration of other risk factors such as the concentration of homocysteine and triglycerides, which is referred to as cardiometabolic risk.
- Consumption of a high-fat meal increased the number of potential risk factors for cardiovascular diseases (homocysteine and triglycerides) compared to a high-carbohydrate meal.
Supplementary Materials
The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/nu14142876/s1, Figure S1: (a) Serum glucose concentration (mg/dL) in the GS and GC groups fasting (time 0′) and after intake (time 30′–240′) of HF meal, (b) Serum glucose concentration (mg/dL) in the GS and GC groups fasting (time 0′) and after intake (time 30′–240′) of HC meal; Figure S2: (a) Serum insulin concentration (IU/mL) in the GS and GC groups fasting (time 0′) and after intake (time 30′–240′) of HF meal, (b) Serum insulin concentration (IU/mL) in the GS and GC groups fasting (time 0′) and after intake (time 30′–240′) of HC meal; Figure S3: (a) Serum triglycerides concentration (mg/dL) in the GS and GC groups fasting (time 0′) and after intake (time 30′–240′) of HF meal, (b) Serum triglycerides concentration (mg/dL) in the GS and GC groups fasting (time 0′) and after intake (time 30′–240′) of HC meal; Figure S4: (a) Serum homocysteine concentration (µmol/l) in the GS and GC groups fasting (time 0′) and after intake (time 30′–240′) of HF meal, (b) Serum homocysteine concentration (µmol/L) in the GS and GC groups fasting (time 0′) and after intake (time 30′–240′) of HC meal; Figure S5: (a) Energy expenditure (kcal/min) in the GS and GC groups fasting (time 0′) and after intake (time 60′–240′) of HF meal, (b) Energy expenditure (kcal/min) in the GS and GC groups fasting (time 0′) and after intake (time 60′–240′) of HC meal; Figure S6: (a) Glucose oxidation (mg/min) in the GS and GC groups fasting (time 0′) and after intake (time 60′–240′) of HF meal, (b) Glucose oxidation (mg/min) in the GS and GC groups fasting (time 0′) and after intake (time 60′–240′) of HC meal; Figure S7: (a) Lipid oxidation (mg/min) in the GS and GC groups fasting (time 0′) and after intake (time 60′–240′) of HF meal, (b) Lipid oxidation (mg/min) in the GS and GC groups fasting (time 0′) and after intake (time 60′–240′) of HC meal.
Author Contributions
Conceptualization, M.G., L.O., A.K. and E.A.-P.; data curation, M.G., L.O., A.K., A.M. and E.A.-P.; formal analysis, M.G. and E.A.-P.; investigation M.G., A.K. and E.A.-P.; methodology, L.O., M.G., A.K., A.M. and E.A.-P.; project administration, L.O., M.G., A.K., A.M. and E.A.-P.; software, A.M. and J.S.-Z.; visualization, L.O., J.S.-Z. and A.M.; writing—original draft, L.O., J.S.-Z. and A.M.; writing—review and editing, M.G., A.K. and E.A.-P. All authors have read and agreed to the published version of the manuscript.
Funding
This study was funded by Ministry of Science and Higher Education, Poland, 2009 (4774/B/P01/2009/37).
Institutional Review Board Statement
This study was approved by the local Bioethics Committee of the Medical University of Bialystok, Poland (No. R-I-002/35/2009).
Informed Consent Statement
Informed consent was obtained from all subjects involved in this study.
Data Availability Statement
Data available on request due to restrictions e.g., privacy or ethical.
Acknowledgments
The authors thank the participants of this study. Trial registration: ClinicalTrials.gov Identifier: NCT03792685.
Conflicts of Interest
The authors declare no conflict of interest.
References
- World Health Organization. Obesity and Overweight. 2020. Available online: https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight (accessed on 7 June 2022).
- Olszanecka-Glinianowicz, M.; Ostrowska, L.; Płaczkiewicz-Jankowska, E. Otyłość. In Interna Szczeklika; Szczeklik, A., Piotr, G., Eds.; Medycyna Praktyczna: Krakow, Poland, 2021; Volume wyd.12, p. 2745. [Google Scholar]
- Jia, A.; Xu, S.; Xing, Y.; Zhang, W.; Yu, X.; Zhao, Y.; Ming, J.; Ji, Q. Prevalence and cardiometabolic risks of normal weight obesity in Chinese population: A nationwide study. Nutr. Metab. Cardiovasc. Dis. 2018, 28, 1045–1053. [Google Scholar] [CrossRef] [PubMed]
- O’Keefe, J.H.; Bell, D.S. Postprandial hyperglycemia/hyperlipidemina (postprandial dysmetabolism) is a cardiovascular risk factor. Am. J. Cardio 2007, 100, 899–904. [Google Scholar] [CrossRef] [PubMed]
- Lairon, D.; Lopez-Miranda, J.; Williams, C. Methodology for studying postprandial lipid metabolism. Eur. J. Clin. Nutr. 2007, 61, 1145–1161. [Google Scholar] [CrossRef] [PubMed]
- Piepoli, M.F.; et. ds. Wytyczne ESC Dotyczące Prewencji Chorób Układu Sercowo-Naczyniowego W Praktyce Klinicznej w 2016 roku. (S.W.G.R.E.T.K.) s. Kardiol Pol. 2016, 74, 821–936. Available online: https://ptkardio.pl/wytyczne/14-wytyczne_esc_dotyczace_prewencji_chorob_ukladu_sercowo_naczyniowego_w_praktyce_klinicznej (accessed on 7 June 2022). [CrossRef] [PubMed] [Green Version]
- Zielińska, M.; Buczkowska-Radlińska, J. The impact of a low-carbohydrate diet on human health. Pomeranian J. Life Sci. 2017, 63, 56–61. [Google Scholar]
- Hu, T.; Bazzano, A.L. The low-carbohydrate diet and cardiovascular risk factors: Evidence from epidemiologic studiem. Nutr. Metab. Cardiovasc Dis. 2014, 24, 337–343. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Bell, D.S.; O’Keefe, J.H.; Jellinger, P. Postprandial dysmetabolism: The missing link between diabetes and cardiovascular events? Endocr. Pract. 2008, 14, 112–124. [Google Scholar] [CrossRef]
- Pappas, C.; Kandaraki, E.A.; Tsirona, S.; Kountouras, D.; Kassi, G.; Diamanti-Kandarakis, E. Postprandial dysmetabolism: Too early or too late? Hormones 2016, 15, 321–344. [Google Scholar] [CrossRef] [Green Version]
- Shi, H.; Seeley, R.J.; Clegg, D.J. Sexual differences in the control of energy homeostasis. Front. Neuroendocr. 2009, 30, 396–404. [Google Scholar] [CrossRef] [Green Version]
- Sugiyama, M.G.; Agellon, L.B. Sex differences in lipid metabolism and metabolic disease risk. Biochem. Cell Biol. 2012, 90, 124–141. [Google Scholar] [CrossRef]
- Ford, E.S. Prevalence of the metabolic syndrome defined by the International Diabetes Federation among adults in the U.S. Diabetes Care 2005, 28, 2745–2749. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Lam, Y.Y.; Ravussin, E. Indirect calorimetry: An indispensable tool to understand and predict obesity. Eur. J. Clin. Nutr. 2017, 71, 318–322. [Google Scholar] [CrossRef] [PubMed]
- Adamska-Patruno, E.; Ostrowska, L.; Golonko, A.; Pietraszewska, B.; Goscik, J.; Kretowski, A.; Gorska, M. Evaluation of Energy Expenditure and Oxidation of Energy Substrates in Adult Males after Intake of Meals with Varying Fat and Carbohydrate Content. Nutrients 2018, 10, 627. [Google Scholar] [CrossRef] [Green Version]
- Urbain, P.; Strom, L.; Morawski, L.; Wehrle, A.; Deibert, P.; Bertz, H. Impact of a 6-week non-energy-restricted ketogenic diet on physical fitness, body composition and biochemical parameters in healthy adults. Nutr. Metab. 2017, 14, 17. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Raben, A.; Agerholm-Larsen, L.; Flint, A.; Holst, J.J.; Astrup, A. Meals with similar energy densities but rich in protein, fat, carbohydrate, or alcohol have different effects on energy expenditure and substrate metabolism but not on appetite and energy intake. Am. J. Clin. Nutr. 2003, 77, 91–100. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- El Khoury, D.; Hwalla, N. Metabolic and Appetite Hormone Responses of Hyperinsulinemic Normoglycemic Males to Meals with Varied Macronutrient Compositions. Ann. Nutr. Metab. 2010, 57, 59–67. [Google Scholar] [CrossRef] [PubMed]
- Wycherley, T.; Brinkworth, G.D.; Keogh, J.B.; Noakes, M.; Buckley, J.; Clifton, P. Long-term effects of weight loss with a very low carbohydrate and low fat diet on vascular function in overweight and obese patients. J. Intern. Med. 2010, 267, 452–461. [Google Scholar] [CrossRef]
- de Roos, N.M.; Bots, M.L.; Siebelink, E.; Schouten, E.; Katan, M.B. Flow-mediated vasodilation is not impaired when HDL-cholesterol is lowered by substituting carbohydrates for monounsaturated fat. Br. J. Nutr. 2001, 86, 181–188. [Google Scholar] [CrossRef] [Green Version]
- Lu, M.; Wan, Y.; Yang, B.; Huggins, C.E.; Li, D. Effects of low-fat compared with high-fat diet on cardiometabolic indicators in people with overweight and obesity without overt metabolic disturbance: A systematic review and meta-analysis of randomised controlled trials. Br. J. Nutr. 2018, 119, 96–108. [Google Scholar] [CrossRef]
- Grabysa, R. Hyperhomocysteinemia: A real risk factor for atheroclerosis? Pol. Prz. Kardiol. 2007, 9, 289–293. [Google Scholar]
- Eckel, N.; Meidtner, K.; Kalle-Uhlmann, T.; Stefan, N.; Schulze, M.B. Metabolically healthy obesity and cardiovascular events: A systematic review and meta-analysis. Eur. J. Prev. Cardiol. 2016, 23, 956–966. [Google Scholar] [CrossRef] [PubMed]
- Ding, C.; Chan, Z.; Chooi, Y.C.; Choo, J.; Sadananthan, S.A.; Chang, A.; Sasikala, S.; Michael, N.; Velan, S.S.; Magkos, F. Regulation of glucose metabolism in nondiabetic, metabolically obese normal-weight Asians. Am. J. Physiol. Metab. 2018, 314, E494–E502. [Google Scholar] [CrossRef] [PubMed]
- Grieb, P.; Kłapcińska, B.; Smol, E.; Pilis, T.; Pilis, W.; Sadowska-Krępa, E.; Sobczak, A.; Bartoszewicz, Z.; Nauman, J.; Stańczak, K.; et al. Long-term consumption of a carbohydrate-restricted diet does not induce deleterious metabolic effects. Nutr. Res. 2008, 28, 825–833. [Google Scholar] [CrossRef] [PubMed]
Figure 1.
The AUC of glucose concentrations in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.5726)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.7004)).
Figure 1.
The AUC of glucose concentrations in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.5726)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.7004)).
Figure 2.
The AUC of insulin concentrations in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.8979)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.0040)).
Figure 2.
The AUC of insulin concentrations in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.8979)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.0040)).
Figure 3.
The AUC of triglyceride concentrations in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.0274)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.0240)).
Figure 3.
The AUC of triglyceride concentrations in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.0274)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.0240)).
Figure 4.
The AUC of homocysteine concentrations in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.0138)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.0040)).
Figure 4.
The AUC of homocysteine concentrations in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.0138)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.0040)).
Figure 5.
The AUC of energy expenditure in the GS and GC groups after HC and HF meals. The results are presented as the mean values. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.6444)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.3693)).
Figure 5.
The AUC of energy expenditure in the GS and GC groups after HC and HF meals. The results are presented as the mean values. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.6444)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.3693)).
Figure 6.
The AUC of glucose oxidation in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.3558)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.2088)).
Figure 6.
The AUC of glucose oxidation in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.3558)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 0.2088)).
Figure 7.
The AUC of lipid oxidation in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.1909)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 1.000)).
Figure 7.
The AUC of lipid oxidation in the GS and GC groups after HC and HF meals. The results are presented as the mean values. * difference between the GS (obese/overweight) and GC (normal body weight) groups after HC meal (high-carbohydrate meal (p = 0.1909)); ** difference between the GS and GC groups after HF meal (high-fat meal (p = 1.000)).
Table 1.
Participant characteristics.
| GS (n = 13) | GC (n = 13) | p | |
|---|---|---|---|
| Age (years) | 37.42 ± 3.15 | 32.10 ± 3.12 | 0.2431 |
| BMI (kg/m2) | 32.36 ± 2.03 | 23.81 ± 0.21 | 0.0003 * |
The results are presented as the mean values ± SE. BMI—body mass index; GS—overweight/obese men; GC—normal body weight men. * p < 0.05.
Table 2.
Composition of standardized meals.
| HC Meal (Nutridrink Fat-Free) Meal Portion: 300 mL | HF Meal (Calogen) Meal Portion: 95 mL | |
|---|---|---|
| Energy value | 450 kcal | 450 kcal |
| Carbohydrates | 100.5 g | 4.0 g |
| % of energy | 89.3% | 4% |
| Mono-and disaccharides | 42.3 g | 3.8 g |
| Glucose | 1.0 g | 0 g |
| Fructose | 0 g | 0 g |
| Lactose | <0.0075 g | 0 g |
| Maltose | 36.3 g | 0 g |
| Saccharose | 5.0 g | 3.8 g |
| Polysaccharides | 57.9 g | 0 g |
| Fats | 0 g | 47.5 g |
| % of energy | 0% | 96% |
| Saturated fat | 0g | 5 g |
| Vegetable fat | 0 g | 42.5 g |
| Milk fat | 0 g | 0 g |
| Monounsaturated fats | 0 g | 28.9 g |
| Polyunsaturated fats | 0 g | 13.6 g |
| Cholesterol | 0 mg | 0 mg |
| Protein | 12 g | 0 g |
| % of energy | 10.7% | 0% |
| % of energy | ||
| Fiber | 0 g | 0 g |
HC meal—high-carbohydrate meal; HF meal—high-fat meal.
Table 3.
Serum concentrations of the biochemical parameters in overweight/obese (GS) men and normal body weight (GC) men on fasting (time 0′) and after (time 30′–240′) high-fat (HF) and high-carbohydrate (HC) meal. (AUC (area under the curve)).
Table 3.
Serum concentrations of the biochemical parameters in overweight/obese (GS) men and normal body weight (GC) men on fasting (time 0′) and after (time 30′–240′) high-fat (HF) and high-carbohydrate (HC) meal. (AUC (area under the curve)).
| High-Fat Meal (HF) | ||||||||||||
| Glucose (mg/dL) | Insulin (IU/mL) | Triglycerides (mg/dL) | Homocysteine (µmol/L) | |||||||||
| Time | GS | GC | p | GS | GC | p | GS | GC | p | GS | GC | p |
| 0′ | 98.4 ± 10.58 | 94.5 ± 8.98 | 0.6622 | 14.7 ± 14.36 | 8.2 ± 2.30 | 0.0812 | 122.0 ± 58.36 | 80.5 ± 35.92 | 0.0377 | 17.3 ± 7.73 | 15.7 ± 5.78 | 0.3172 |
| 30′ | 95.3 ± 10.37 | 92.7 ± 9.29 | 0.8772 | 21.3 ± 21.88 | 10.1 ± 3.89 | 0.0355 | 127.1 ± 65.81 | 81.3 ± 37.01 | 0.0256 | 16.9 ± 6.03 | 13.8 ± 2.53 | 0.0686 |
| 60′ | 88.6 ± 12.44 | 89.9 ± 7.92 | 0.5041 | 21.1 ± 18.12 | 9.6 ± 3.72 | 0.0024 | 126.3 ± 77.72 | 84.3 ± 34.47 | 0.0576 | 24.7 ± 14.01 | 14.4 ± 2.35 | 0.0292 |
| 120′ | 89.7 ± 9.90 | 89.7 ± 6.40 | 0.4399 | 17.6 ± 10.77 | 8.4 ± 2.13 | 0.0065 | 166.3 ± 97.78 | 109.9 ± 34.51 | 0.0158 | 21.5 ± 6.91 | 13.0 ± 2.60 | 0.0011 |
| 180′ | 91.6 ± 9.26 | 88.0 ± 5.78 | 0.4257 | 15.4 ± 11.45 | 8.1 ± 2.66 | 0.0159 | 205.9 ± 91.93 | 136.5 ± 48.25 | 0.0311 | 22.9 ± 14.81 | 14.6 ± 4.82 | 0.2701 |
| 240′ | 90.9 ± 7.18 | 89.3 ± 6.77 | 0.9794 | 12.4 ± 8.27 | 8.5 ± 3.28 | 0.2184 | 206.6 ± 91.53 | 148.5 ± 72.81 | 0.1508 | 23.2 ± 10.80 | 14.7 ± 2.88 | 0.0377 |
| AUC | 21658 ± 334 | 21,593 ± 442 | 0.7004 | 4171 ± 857 | 2113 ± 157 | 0.0040 | 39,867 ± 5453 | 26,685 ± 2713 | 0.0240 | 5370 ± 539 | 3437 ± 147 | 0.0040 |
| High-Carbohydrate Meal (HC) | ||||||||||||
| Glucose (mg/dL) | Insulin (IU/mL) | Triglycerides (mg/dL) | Homocysteine (µmol/L) | |||||||||
| Time | GS | GC | p | GS | GC | p | GS | GC | p | GS | GC | p |
| 0′ | 96.2 ± 9.18 | 91.6 ± 18.31 | 0.6254 | 14.8 ± 14.10 | 10.2 ± 5.20 | 0.6628 | 113.5 ± 41.25 | 75.3 ± 41.03 | 0.0294 | 16.8 ± 4.17 | 13.2 ± 2.49 | 0.0221 |
| 30′ | 158.0 ± 25.65 | 152.3 ± 30.28 | 0.9794 | 181.1 ± 283.38 | 86.2 ± 31.06 | 0.7778 | 116.6 ± 39.65 | 77.0 ± 42.18 | 0.0294 | 19.4 ± 9.10 | 13.2 ± 4.02 | 0.0042 |
| 60′ | 169.3 ± 46.81 | 149.3 ± 31.33 | 0.3166 | 238.1 ± 342.86 | 120.8 ± 86.53 | 0.9795 | 118.3 ± 47.64 | 74.5 ± 42.35 | 0.0190 | 15.7 ± 7.35 | 13.8 ± 5.55 | 0.3107 |
| 120′ | 140.6 ± 51.61 | 127.0 ± 26.94 | 0.6440 | 141.1 ± 197.22 | 84.1 ± 41.21 | 0.7388 | 105.5 ± 45.08 | 62.9 ± 38.55 | 0.0119 | 19.0 ± 11.41 | 12.3 ± 1.74 | 0.0255 |
| 180′ | 105.3 ± 19.81 | 104.6 ± 25.86 | 0.8174 | 42.4 ± 33.24 | 45.9 ± 32.18 | 0.6628 | 102.8 ± 49.75 | 63.0 ± 42.15 | 0.0190 | 19.6 ± 11.12 | 12.6 ± 3.20 | 0.0190 |
| 240′ | 78.7 ± 19.00 | 77.1 ± 18.98 | 0.9386 | 17.1 ± 13.30 | 13.6 ± 6.02 | 0.8979 | 98.7 ± 51.86 | 71.5 ± 51.03 | 0.0908 | 15.1 ± 8.97 | 12.4 ± 3.27 | 0.5787 |
| AUC | 30,482 ± 1426 | 28,882 ± 1322 | 0.5726 | 27,907 ± 9545 | 16,396 ± 1784 | 0.8979 | 25,995 ± 3046 | 16,502 ± 2772 | 0.0274 | 4323 ± 511 | 3090 ± 141 | 0.0138 |
Table 4.
Energy expenditure (kcal/min), glucose and fat oxidation (mg/min) in GS (overweight/obesity) group and GC (normal body weight) group on fasting (time 0′) and after (time 60′–240′) a high-fat (HF) meal and a high-carbohydrate (HC) meal. (AUC (area under the curve)).
Table 4.
Energy expenditure (kcal/min), glucose and fat oxidation (mg/min) in GS (overweight/obesity) group and GC (normal body weight) group on fasting (time 0′) and after (time 60′–240′) a high-fat (HF) meal and a high-carbohydrate (HC) meal. (AUC (area under the curve)).
| High-Fat Meal (HF) | |||||||||
| Energy Expenditure (kcal/min) | Glucose Oxidation (mg/min) | Fat Oxidation (mg/min) | |||||||
| Time | GS | GC | p | GS | GC | p | GS | GC | p |
| 0′ | 1.332 ± 0.25 | 1.267 ± 0.24 | 0.3970 | 41.3 ± 47.76 | 34.0 ± 43.71 | 0.5552 | 71.4 ± 36.46 | 56.4 ± 33.22 | 0.2811 |
| 60′ | 1.333 ± 0.27 | 1.263 ± 0.19 | 0.6628 | 61.4 ± 66.25 | 34.4 ± 45.07 | 0.2084 | 82.4 ± 48.55 | 87.3 ± 31.98 | 0.8979 |
| 120′ | 1.335 ± 0.23 | 1.269 ± 0.22 | 0.2181 | 43.9 ± 48.04 | 34.3 ± 40.93 | 0.6628 | 91.5 ± 40.76 | 90.1 ± 29.02 | 0.9590 |
| 180′ | 1.336 ± 0.26 | 1.217 ± 0.10 | 0.1237 | 24.9 ± 19.29 | 27.6 ± 41.69 | 0.5724 | 103.0 ± 32.43 | 92.0 ± 27.96 | 0.3426 |
| 240′ | 1.339 ± 0.24 | 1.327 ± 0.20 | 0.2928 | 23.5 ± 9.66 | 31.9 ± 45.45 | 0.5046 | 105.5 ± 32.80 | 94.4 ± 30.18 | 0.4263 |
| AUC | 325.64 ± 16.478 | 302.87 ± 9.526 | 0.3693 | 9775 ± 1987 | 7765 ± 2738 | 0.2088 | 21,936 ± 2305 | 20,699 ± 1937 | 1.0000 |
| High-Carbohydrate Meal (HC) | |||||||||
| Energy Expenditure (kcal/min) | Glucose Oxidation (mg/min) | Fat Oxidation (mg/min) | |||||||
| Time | GS | GC | p | GS | GC | p | GS | GC | p |
| 0′ | 1.329 ± 0.22 | 1.222 ± 0.15 | 0.1369 | 23.9 ± 22.60 | 28.6 ± 22.5 | 0.4265 | 87.7 ± 28.40 | 66.2 ± 26.50 | 0.1061 |
| 60′ | 1.447 ± 0.30 | 1.338 ± 0.09 | 0.5381 | 46.0 ± 55.44 | 46.7 ± 56.01 | 0.9386 | 93.4 ± 34.56 | 77.7 ± 23.98 | 0.1822 |
| 120′ | 1.395 ± 0.29 | 1.311 ± 0.10 | 0.7583 | 68.7 ± 60.23 | 76.2 ± 49.84 | 0.3692 | 78.5 ± 28.98 | 63.6 ± 22.98 | 0.1689 |
| 180′ | 1.325 ± 0.26 | 1.220 ± 0.14 | 0.6816 | 62.9 ± 63.27 | 67.6 ± 53.88 | 0.3972 | 71.7 ± 26.32 | 57.5 ± 24.06 | 0.1689 |
| 240′ | 1.316 ± 0.29 | 1.240 ± 0.12 | 0.7583 | 42.5 ± 30.08 | 35.0 ± 46.29 | 0.0479 | 84.7 ± 36.40 | 77.6 ± 22.67 | 0.6138 |
| AUC | 329.48 ± 18.328 | 306.14 ± 7.191 | 0.6444 | 12,665 ± 3013 | 13,351 ± 2689 | 0.3558 | 19,799 ± 1901 | 16,253 ± 1322 | 0.1909 |
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. |
© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
Share and Cite
MDPI and ACS Style
Ostrowska, L.; Smarkusz-Zarzecka, J.; Muszyńska, A.; Adamska-Patruno, E.; Górska, M.; Krętowski, A. High-Fat or High-Carbohydrate Meal—Does It Affect the Metabolism of Men with Excess Body Weight? Nutrients 2022, 14, 2876. https://doi.org/10.3390/nu14142876
AMA Style
Ostrowska L, Smarkusz-Zarzecka J, Muszyńska A, Adamska-Patruno E, Górska M, Krętowski A. High-Fat or High-Carbohydrate Meal—Does It Affect the Metabolism of Men with Excess Body Weight? Nutrients. 2022; 14(14):2876. https://doi.org/10.3390/nu14142876
Chicago/Turabian StyleOstrowska, Lucyna, Joanna Smarkusz-Zarzecka, Anna Muszyńska, Edyta Adamska-Patruno, Maria Górska, and Adam Krętowski. 2022. "High-Fat or High-Carbohydrate Meal—Does It Affect the Metabolism of Men with Excess Body Weight?" Nutrients 14, no. 14: 2876. https://doi.org/10.3390/nu14142876
Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.
