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Nutrients
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Pathophysiology of Glucose and Lipid Metabolism in Noncommunicable Diseases (NCDs)
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Pathophysiology of Glucose and Lipid Metabolism in Noncommunicable Diseases (NCDs)

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

Deadline for manuscript submissions: closed (5 March 2026) | Viewed by 4672

Special Issue Editor

Dr. Takao Kimura

E-Mail Website
Guest Editor
1. Department of Integrated Health Science, Graduate School of Food and Population Health Science, Gunma University, Aramaki-Machi 4-2, Maebashi 371-8510, Gunma, Japan
2. General Health Support Center, Gunma University, Aramaki-Machi 4-2, Maebashi 371-8510, Gunma, Japan
Interests: obesity; glucose metabolism; insulin resistance; lipid metabolism; exercise; food science; cancer; CKD; MASLD; osteoporosis; postmenopausal; sarcopenia; flail; mental stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

According to the WHO, noncommunicable diseases (NCDs) accounted for 75% of all deaths worldwide in 2021. Among NCDs, the leading cause of death is cardiovascular disease, followed by cancer, chronic respiratory disease, and diabetes-related diseases. NCDs, which are chronic diseases, are the result of a combination of genetic, physiological, environmental, and behavioral factors [1,2]. Therefore, the prevention and early detection of NCDs through checkups and screening tests is important. To achieve early NCD detection, it is necessary to clarify NCD pathophysiology. The four major metabolic changes that predispose people to NCDs are (1) hypertension, (2) obesity/overweight, (3) elevated blood glucose levels, and (4) dyslipidemia. A key approach to NCD control is to focus on risk factor mitigation [1]. Low-cost solutions exist for governments and other stakeholders to reduce common modifiable risk factors. Monitoring the progress and trends in NCDs and their risk factors is important to guide policies and priorities [1]. NCD management involves detecting, screening, and treating these diseases and providing palliative care for those in need. High-impact and essential NCD interventions can be delivered through primary healthcare approaches to strengthen early detection and timely treatment. Establishing effective strategies to combat the ever-increasing number of NCDs remains an urgent global issue [1]. This Special Issue aims to clarify the changes in glucose and lipid metabolism involved in NCD pathogenesis through research on cells, animals, and humans. Researchers, please submit your latest research findings on glucose and lipid metabolism and NCDs. Research on atherosclerotic diseases, cancer, chronic respiratory diseases, diabetes-related diseases, and mental illnesses is welcome. Disorders of glucose and lipid metabolism are commonly seen in CKD, MSLD, depression, and postmenopausal women and are closely related to osteoporosis. These diseases ultimately lead to sarcopenia and frailty, resulting in a shortened healthy life expectancy. This Special Issue covers diseases across all specialties involving glucose and lipid metabolism and the impact of dietary factors. We look forward to receiving your submissions.

References

  1. Noncommunicable Diseases: https://www.who.int/news-room/fact-sheets/detail/noncommunicable-diseases.
  2. Global Burden of Disease Collaborative Network: https://vizhub.healthdata.org/gbd-results/.

Dr. Takao Kimura
Guest Editor

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • glucose metabolism
  • lipid metabolism
  • nutritional screening
  • atherosclerotic diseases
  • cancer
  • chronic respiratory diseases
  • diabetes-related diseases
  • mental illnesses
  • obesity
  • overweight

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Published Papers (3 papers)

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Research

24 pages, 2905 KB  
Article
Cafeteria and Fast-Food Diets Induce Neuroinflammation, Social Deficits, but a Different Cardiometabolic Phenotype
by Andrej Feješ, Petronela Sušienková, Lucia Mihalovičová, Veronika Kunšteková, Radana Gurecká, Veronika Borbélyová, Peter Celec and Katarína Šebeková
Nutrients 2025, 17(22), 3614; https://doi.org/10.3390/nu17223614 - 19 Nov 2025
Cited by 1 | Viewed by 1271
Abstract
Background: Obesity is a risk factor for several non-communicable diseases and premature death. The Western-type diet, rich in calories and diverse in tastes, smells, and textures, promotes the onset and progression of obesity. We compared the effects of two Western-style palatable obesogenic diets—the [...] Read more.
Background: Obesity is a risk factor for several non-communicable diseases and premature death. The Western-type diet, rich in calories and diverse in tastes, smells, and textures, promotes the onset and progression of obesity. We compared the effects of two Western-style palatable obesogenic diets—the cafeteria (CAF) diet, which allows for self-selection of calorie-dense food items consumed by humans, and the fast-food diet (FFD)—composed of a fixed combination of cheeseburgers and fries—on the manifestation of obesity-related complications. Methods: 3-month-old female rats consumed either the control (CTRL), FFD, or CAF diet for 12 months. Body weight was monitored weekly. At the end of the experiment, rats underwent metabolic and behavioral testing. Cardiometabolic markers and those characterizing glycoxidative and carbonyl stress, inflammatory status, and tryptophan metabolism were determined. Results: The CAF rats gain most weight (CTRL: +111 ± 40 g; FFD: +211 ± 77 g; CAF: 316 ± 87 g). CAF feeding produced a classical metabolic syndrome–like profile with severe obesity, insulin resistance, dyslipidemia, and liver steatosis, whereas the FFD model led to moderate obesity with preserved insulin sensitivity but elevated blood pressure and hepatic cholesterol accumulation. Thus, the CAF group developed a severe metabolic syndrome-like pathology assessed as continuous metabolic syndrome z-core (CTRL: −2.3 ± 1.0; FFD: −0.4 ± 1.9; CAF: 3.0 ± 2.4). Despite these differences, both diets promoted neuroinflammation and social deficits, likely mediated through gut microbiota–derived metabolites such as 5-HIAA and indoxyl sulfate. Conclusions: In female rats, self-selected CAF diet drives more severe and distinct pattern of metabolic syndrome-like pathology than a fixed FFD. Full article
(This article belongs to the Special Issue Pathophysiology of Glucose and Lipid Metabolism in Noncommunicable Diseases (NCDs))
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13 pages, 1694 KB  
Article
Synergistic Association of Glycemic Variability and Severe Vitamin D Deficiency with Proliferative Diabetic Retinopathy
by Nejla Dervis, Simona Carniciu, Alina Spinean and Sanda Jurja
Nutrients 2025, 17(20), 3210; https://doi.org/10.3390/nu17203210 - 13 Oct 2025
Cited by 1 | Viewed by 917
Abstract
Background: Oscillating hyperglycemia (glycemic variability) and vitamin D deficiency each damage the retinal microvasculature, yet their combined effect on sight-threatening proliferative diabetic retinopathy (PDR) is uncertain. Objective: To determine whether high GV and severe vitamin D deficiency independently, and additively, associate with retinal [...] Read more.
Background: Oscillating hyperglycemia (glycemic variability) and vitamin D deficiency each damage the retinal microvasculature, yet their combined effect on sight-threatening proliferative diabetic retinopathy (PDR) is uncertain. Objective: To determine whether high GV and severe vitamin D deficiency independently, and additively, associate with retinal neovascularization in adults with diabetes. Materials and Methods: We conducted a cross-sectional study between January 2025 and June 2025 in 58 adults with diabetes at Constanța County Emergency Hospital, Romania. GV was classified as high (coefficient of variation > 36% or SMBG-SD > 50 mg/dL) or low. Serum 25-hydroxy-vitamin D [25(OH)D] was measured; severe deficiency < 10 ng/mL. Dilated funduscopy graded retinopathy as non-proliferative (NPDR) or proliferative (PDR). Multivariable logistic regression adjusted for HbA1c, diabetes duration, BMI, smoking, triglycerides and therapy. Results: From 58 adults (mean ± SD 59 ± 11 years), high GV characterized 29/58 participants (50%). Severe vitamin D deficiency was more frequent in the GV-high group (45% vs. 31%). PDR prevalence was 48% in GV-high and 31% in GV-low patients. After adjustment, high GV (adjusted OR 2.31, 95% CI 1.05–5.09) and severe vitamin D deficiency (OR 2.04, 95% CI 0.98–4.25) each predicted PDR. Concomitant exposure to both stressors conferred 3.9-fold higher odds of PDR (OR 3.88, 95% CI 1.35–11.1). No interaction term reached significance (p = 0.21), indicating additive effects. Conclusions: High GV and severe vitamin D deficiency independently and additively associate with PDR. Screening for both parameters may enhance risk stratification of PDR. Within adults with diabetes, high glycemic variability and severe vitamin D deficiency were each associated with higher odds of PDR after adjustment for HbA1c, diabetes duration, BMI, smoking, triglycerides, and treatment pattern; their effects appeared additive rather than multiplicative. These findings reflect associations within diabetes and do not imply that vitamin D deficiency produces retinopathy in euglycemic individuals. Full article
(This article belongs to the Special Issue Pathophysiology of Glucose and Lipid Metabolism in Noncommunicable Diseases (NCDs))
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18 pages, 276 KB  
Article
Reciprocal Fluctuations in Lipoprotein Lipase, Glycosylphosphatidylinositol-Anchored High-Density Lipoprotein-Binding Protein 1, and Hepatic Triglyceride Lipase Levels in the Peripheral Bloodstream Are Correlated with Insulin Resistance
by Takumi Nagasawa, Koji Sakamaki, Akihiro Yoshida, Hiroki Machida, Fumitaka Murakami, Mari Hashimoto, Takahito Shinohara, Masami Murakami, Katsuhiko Tsunekawa and Takao Kimura
Nutrients 2025, 17(11), 1880; https://doi.org/10.3390/nu17111880 - 30 May 2025
Cited by 5 | Viewed by 1941
Abstract
Background/Objectives: This study aimed to identify the regulatory system of lipoprotein lipase (LPL), glycosylphosphatidylinositol-anchored high-density lipoprotein (HDL)-binding protein 1 (GPIHBP1), and hepatic triglyceride lipase (HTGL) in the peripheral bloodstream. Methods: In total, 207 individuals (100 males and 107 females) who were diagnosed [...] Read more.
Background/Objectives: This study aimed to identify the regulatory system of lipoprotein lipase (LPL), glycosylphosphatidylinositol-anchored high-density lipoprotein (HDL)-binding protein 1 (GPIHBP1), and hepatic triglyceride lipase (HTGL) in the peripheral bloodstream. Methods: In total, 207 individuals (100 males and 107 females) who were diagnosed with normal glucose tolerance or prediabetes during their comprehensive health checkup were investigated. Results: Circulating LPL levels were positively correlated with the GPIHBP1 and HDL-cholesterol (HDL-C) levels, and negatively correlated with body mass index (BMI), waist circumference (WC), Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) scores, triglyceride–glucose index, and triglyceride, fasting insulin, ferritin, and C-reactive protein (CRP) levels. The GPIHBP1 level was positively correlated with LPL and HTGL levels, and negatively correlated with estimated glomerular filtration rate (eGFR). The HTGL level was positively correlated with BMI, WC, HOMA-IR score, and GPIHBP1, low-density lipoprotein cholesterol (LDL-C), fasting insulin, and ferritin levels. Meanwhile, it was negatively correlated with HDL-C levels. The multiple regression analysis revealed that the circulating LPL level was independently affected by BMI, red blood cell (RBC) count, GPIHBP1, fasting plasma glucose (FPG), fasting insulin, HDL-C, CRP, and ferritin levels. The GPIHBP1 level was independently affected by age, eGFR, FPG, LPL, and HTGL levels and RBC count. The HTGL level was independently affected by WC, GPIHBP1 and LDL-C levels. Conclusions: LPL and HTGL levels reflect insulin resistance. In particular, individuals with a greater insulin resistance present with a lower LPL level and a higher HTGL level. An increased GPIHBP1 level might compensate for decreased LPL levels due to insulin resistance. Full article
(This article belongs to the Special Issue Pathophysiology of Glucose and Lipid Metabolism in Noncommunicable Diseases (NCDs))
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