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Unbalanced Diets: High-Fat, High-Sucrose and High-Protein Diets

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (25 August 2022) | Viewed by 11939

Special Issue Editors


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Guest Editor
1. Laboratory of Molecular Biology, Nutrition and Biotechnology (Nutrigenomics, Biomarkers and Risk Evaluation Group), University of the Balearic Islands, 07122 Palma, Spain
2. Health Research Institute of the Balearic Islands (IdISBa), 07120 Palma, Spain
3. CIBER of Physiopathology of Obesity and Nutrition (CIBEROBN), Carlos III Health Institute (ISCIII), 28029 Madrid, Spain
4. Alimentómica S.L. Camí de na Pontons. s/n (Pol.11, Parc 3), 07310 Campanet, Spain
Interests: obesity; diets; metabolic alterations; nutrigenomics; nutrigenetics; bioactive compounds
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
1. Laboratory of Molecular Biology, Nutrition and Biotechnology, University of the Balearic Islands (UIB), Palma, Illes Balears, Spain
2. Health Research Institute of the Balearic Islands (IdISBa), Palma, Illes Balears, Spain
3. CIBER de Fisiopatología de la Obesidad y Nutrición (CIBERobn), ES-07122 Palma, Spain
4. Alimentómica SL., Palma, Illes Balears, Spain
Interests: obesity; diets; metabolic alterations; perinatal nutrition; metabolic programming and regulation; nutrigenomics; bioactive compounds
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Maintaining a balanced diet is essential to reach and preserve a healthy metabolic status. In contrast, the consumption of an unbalanced diet is associated with the development of obesity and other metabolic alterations. Thus, the intake of high-fat, high-sucrose (or both) and high-protein diets are associated not only with metabolic status perse but also with many diseases, from various types of cancers to neurological diseases and cognitive disfunctions, diseases associated with the locomotor system, etc. However, are unbalanced diets always a bad option? Ketodiets, diets low in carbohydrates and high in protein or fat, have been useful for weight loss and garnered excellent results for the control of diabetes. Knowing the mechanism/s through which these diets modulate metabolic and molecular pathways is crucial to understanding how unbalanced diets can affect human health. Moreover, beyond the effect/s of consuming these diets on the individual's own health, the consequences of the continued maternal intake of unbalanced diets during pregnancy or lactation on the health of offspring is not well known and deserves further study. In this Special Issue of Nutrients, we will focus on how various unbalanced diets (on macronutrients content) alter a healthy status or could be used in specific situations to improve metabolic-altered conditions.

Dr. Barbara Reynés
Dr. Mariona Palou
Guest Editors

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Keywords

  • unbalanced diets
  • obesity
  • metabolic disorders

Published Papers (5 papers)

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Research

18 pages, 1824 KiB  
Article
Characterization of the Cafeteria Diet as Simulation of the Human Western Diet and Its Impact on the Lipidomic Profile and Gut Microbiota in Obese Rats
by Ana Laura de la Garza, Alejandra Mayela Martínez-Tamez, Anael Mellado-Negrete, Sofía Arjonilla-Becerra, Gloria Itzel Peña-Vázquez, Luis Martín Marín-Obispo and Carmen Hernández-Brenes
Nutrients 2023, 15(1), 86; https://doi.org/10.3390/nu15010086 - 24 Dec 2022
Cited by 5 | Viewed by 3188
Abstract
The obesity pandemic has been strongly associated with the Western diet, characterized by the consumption of ultra-processed foods. The Western lifestyle causes gut dysbiosis leading to impaired fatty acid metabolism. Therefore, this study aimed to evaluate shifts in gut microbiota and correlate these [...] Read more.
The obesity pandemic has been strongly associated with the Western diet, characterized by the consumption of ultra-processed foods. The Western lifestyle causes gut dysbiosis leading to impaired fatty acid metabolism. Therefore, this study aimed to evaluate shifts in gut microbiota and correlate these with serum fatty acid profiles in male Wistar rats fed a cafeteria diet. Ten male rats were fed with standard diet (CTL, n = 5) and cafeteria diet (CAF, n = 5) for fifteen weeks. Body weight and food intake were recorded once and three times per week, respectively. At the end of the study, fresh fecal samples were collected, tissues were removed, and serum samples were obtained for further analyses. Gut microbiota was analyzed by sequencing the V3-V4 region of 16S rRNA gene. Serum fatty acid profiles were fractioned and quantified via gas chromatography. The CAF diet induced an obese phenotype accompanied by impaired serum fatty acids, finding significantly higher proportions of total saturated fatty acids (SFAs) and C20:3 n-6, and lower C18:1 n-7 and C18:3 n-3 in the phospholipid (PL) fraction. Furthermore, circulating C10:0, total n-3 and n-7 decreased and total monounsaturated fatty acids (MUFAs), including oleic acid C18:1 n-9, increased in the cholesterol ester (CE) fraction. The obesity metabotype may be mediated by gut dysbiosis caused by a cafeteria diet rich in C16:0, C18:0, C18:1 n-9 and C18:2 n-6 fatty acids resulting in a 34:1 omega-6/omega-3 ratio. Therefore, circulating C10:0 was associated with several genera bacteria such as Prevotella (positive) and Anaerotruncus (negative). Two classes of Firmicutes, Bacilli and Erysipelotrichi, were positively correlated with PL- C20:3 n-6 and CE- 18:1 n-9, respectively. TM7 and Bacteroidetes were inversely correlated with PL-SFAs and CE- 18:2 n-6, respectively. Full article
(This article belongs to the Special Issue Unbalanced Diets: High-Fat, High-Sucrose and High-Protein Diets)
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23 pages, 2301 KiB  
Article
Maternal Supplementation with a Cocoa Extract during Lactation Deeply Modulates Dams’ Metabolism, Increases Adiponectin Circulating Levels and Improves the Inflammatory Profile in Obese Rat Offspring
by Roger Mariné-Casadó, Cristina Domenech-Coca, Anna Crescenti, Miguel Ángel Rodríguez Gómez, Josep Maria Del Bas, Lluís Arola, Noemí Boqué and Antoni Caimari
Nutrients 2022, 14(23), 5134; https://doi.org/10.3390/nu14235134 - 03 Dec 2022
Cited by 1 | Viewed by 1926
Abstract
High-flavonoid cocoa consumption has been associated with beneficial properties. However, there are scarce data concerning the effects of maternal cocoa intake on dams and in their progeny. Here, we evaluated in rats whether maternal supplementation with a high-flavan-3-ol cocoa extract (CCX) during lactation [...] Read more.
High-flavonoid cocoa consumption has been associated with beneficial properties. However, there are scarce data concerning the effects of maternal cocoa intake on dams and in their progeny. Here, we evaluated in rats whether maternal supplementation with a high-flavan-3-ol cocoa extract (CCX) during lactation (200 mg.kg−1.day−1) produced beneficial effects on dams and in their normoweight (STD-CCX group) and cafeteria-fed obese (CAF-CCX group) adult male offspring. Maternal intake of CCX significantly increased the circulating levels of adiponectin and decreased the mammary gland lipid content of dams. These effects were accompanied by increased energy expenditure and circulating free fatty acids, as well as by a higher expression of lipogenic and adiponectin-related genes in their mammary glands, which could be related to a compensatory mechanism to ensure enough lipid supply to the pups. CCX consumption programmed both offspring groups towards increased plasma total adiponectin levels, and decreased liver weight and lean/fat ratio. Furthermore, CAF-CCX progeny showed an improvement of the inflammatory profile, evidenced by the significant decrease of the monocyte chemoattractant protein-1 (MCP-1) circulating levels and the mRNA levels of the gene encoding the major histocompatibility complex, class II invariant chain (Cd74), a marker of M1 macrophage phenotype, in the epididymal white adipose tissue. Although further studies are needed, these findings can pave the way for using CCX as a nutraceutical supplement during lactation. Full article
(This article belongs to the Special Issue Unbalanced Diets: High-Fat, High-Sucrose and High-Protein Diets)
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15 pages, 3642 KiB  
Article
Maternal Low-Protein Diet during Puberty and Adulthood Aggravates Lipid Metabolism of Their Offspring Fed a High-Fat Diet in Mice
by Xiaohua Huang, Yong Zhuo, Dandan Jiang, Yingguo Zhu, Zhengfeng Fang, Lianqiang Che, Yan Lin, Shengyu Xu, Lun Hua, Yuanfeng Zou, Chao Huang, Lixia Li, De Wu and Bin Feng
Nutrients 2022, 14(19), 4057; https://doi.org/10.3390/nu14194057 - 29 Sep 2022
Viewed by 1988
Abstract
A maternal low-protein (LP) diet during gestation and/or lactation results in metabolic syndrome in their offspring. Here, we investigated the effect of maternal LP diet during puberty and adulthood on the metabolic homeostasis of glucose and lipids in offspring. Female mice were fed [...] Read more.
A maternal low-protein (LP) diet during gestation and/or lactation results in metabolic syndrome in their offspring. Here, we investigated the effect of maternal LP diet during puberty and adulthood on the metabolic homeostasis of glucose and lipids in offspring. Female mice were fed with normal-protein (NP) diet or a LP diet for 11 weeks. Male offspring were then fed with a high-fat diet (NP-HFD and LP-HFD groups) or standard chow diet (NP-Chow and LP-Chow groups) for 4 months. Results showed that maternal LP diet during puberty and adulthood did not alter the insulin sensitivity and hepatic lipid homeostasis of their offspring under chow diet, but aggravated insulin resistance, hepatic steatosis, and hypercholesterolemia of offspring in response to a post-weaning HFD. Accordingly, transcriptomics study with offspring’s liver indicated that several genes related to glucose and lipid metabolism, including lipoprotein lipase (Lpl), long-chain acyl-CoA synthetase 1 (Acsl1), Apoprotein A1 (Apoa1), major urinary protein 19 (Mup19), cholesterol 7α hydroxylase (Cyp7a1) and fibroblast growth factor 1 (Fgf1), were changed by maternal LP diet. Taken together, maternal LP diet during puberty and adulthood could disarrange the expression of metabolic genes in the liver of offspring and aggravate insulin resistance and hepatic steatosis in offspring fed a HFD. Full article
(This article belongs to the Special Issue Unbalanced Diets: High-Fat, High-Sucrose and High-Protein Diets)
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17 pages, 3615 KiB  
Article
Perinatal Treatment with Leptin, but Not Celastrol, Protects from Metabolically Obese, Normal-Weight Phenotype in Rats
by Bàrbara Reynés, Margalida Cifre, Andreu Palou and Paula Oliver
Nutrients 2022, 14(11), 2277; https://doi.org/10.3390/nu14112277 - 29 May 2022
Cited by 2 | Viewed by 1981
Abstract
Perinatal nutrition has a well-known influence on obesity susceptibility. We previously demonstrated the protective anti-obesity effects of perinatal leptin administration. Celastrol is a natural compound acting as a leptin sensitizer with anti-obesity effects when administered in adult animals. Here, we aimed to determine [...] Read more.
Perinatal nutrition has a well-known influence on obesity susceptibility. We previously demonstrated the protective anti-obesity effects of perinatal leptin administration. Celastrol is a natural compound acting as a leptin sensitizer with anti-obesity effects when administered in adult animals. Here, we aimed to determine if perinatal treatment with leptin, celastrol, or their combination was able to improve metabolic health in animals fed an isocaloric high-fat (HF) diet. Leptin and/or celastrol or their vehicle were administered orally to rats during the suckling period. After weaning, animals were chronically pair-fed with an HF diet provided isocaloric to the intake of a normal-fat diet by control animals to avoid obesity. Isocaloric HF feeding in vehicle-treated animals resulted in metabolic features characteristic of the metabolically obese, normal-weight (MONW) phenotype, i.e., obesity-related disturbances without increased body weight. Leptin treatment prevented liver fat deposition and insulin resistance, induced greater insulin and leptin signaling capacity, decreased gene expression of orexigenic signals at the hypothalamic level, and induced browning in retroperitoneal adipose tissue. However, celastrol treatment did not provide any protective effect and resulted in greater size of the retroperitoneal adipose depot, higher circulating glucose and insulin levels, and decreased leptin sensitivity capacity in adipose tissue. The co-administration of leptin ameliorated the negative effects of celastrol on the retroperitoneal depot, inducing browning and decreasing its size. In conclusion, the perinatal administration of leptin, but not celastrol, provided protection against the consequences of dietary unbalances leading to an MONW phenotype in adulthood. Full article
(This article belongs to the Special Issue Unbalanced Diets: High-Fat, High-Sucrose and High-Protein Diets)
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15 pages, 2268 KiB  
Article
Maternal Consumption of a Cafeteria Diet during Lactation Leads to Altered Diet-Induced Thermogenesis in Descendants after Exposure to a Western Diet in Adulthood
by Catalina Amadora Pomar, Catalina Picó, Andreu Palou and Juana Sánchez
Nutrients 2022, 14(9), 1958; https://doi.org/10.3390/nu14091958 - 07 May 2022
Cited by 3 | Viewed by 2054
Abstract
This study investigates the ability of a maternal cafeteria diet during lactation to program brown adipose tissue (BAT) metabolic responses to an obesogenic diet re-exposure in the adult offspring after consuming a standard diet (SD). Nursing rats were fed an SD or a [...] Read more.
This study investigates the ability of a maternal cafeteria diet during lactation to program brown adipose tissue (BAT) metabolic responses to an obesogenic diet re-exposure in the adult offspring after consuming a standard diet (SD). Nursing rats were fed an SD or a cafeteria diet during lactation. Their offspring (O-C and O-CAF, respectively) were weaned onto an SD, and at 16 weeks of age they were switched to a Western diet until week 24. Gene and protein expression in BAT were measured at PN22 and at 24 weeks. At PN22, compared to controls, O-CAF rats displayed lower mRNA levels of lipogenesis-related genes (Fasn), and higher expression of genes related to lipolysis (Pnpla2), fatty acid uptake (Cd36, Lpl), and oxidation (Cpt1b). Additionally, O-CAF animals displayed increased mRNA levels of Adrb3, Ucp1, and Cidea. In adulthood, these animals maintained lower mRNA levels of lipogenesis-related genes (Pparg, Srebf1, Fasn), but displayed lower expression of genes related to fatty acid uptake (Cd36), fatty acid oxidation (Cpt1b), lipolysis (Pnpla2), Adrb3, Ucp1, and Cidea. Thus, exposure to an obesogenic diet in nursing rats can affect long-term lipid metabolism and attenuate diet-induced thermogenesis in BAT in response to a new obesogenic dietary challenge later in life. Full article
(This article belongs to the Special Issue Unbalanced Diets: High-Fat, High-Sucrose and High-Protein Diets)
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