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Impact of Nutritional Regulation on the Control of Glucose Homeostasis and Type 2 Diabetes Mellitus

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

Deadline for manuscript submissions: 5 July 2024 | Viewed by 5748

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Special Issue Editors

Dr. Shaodong Guo

E-Mail Website
Guest Editor

Department of Nutrition, Texas A&M University, College Station, TX 77843, USA
Interests: insulin resistance; insulin signaling; metabolism; lipid metabolism; glucose metab-olism; energy metabolism; metabolic diseases; metabolic endocrinology

Dr. Wanbao Yang

E-Mail Website
Co-Guest Editor

Department of Nutrition, Texas A&M University, College Station, TX 77843, USA
Interests: insulin resistance; glucose and lipid metabolism; sexual dimorphism

Special Issue Information

Dear Colleagues,

Type 2 diabetes mellitus (T2DM) is an increasing global health issue, highly associated with the epidemic of obesity. In healthy individuals, glucose homeostasis is tightly regulated by insulin and its counterregulatory hormones. Individuals with T2DM show insulin resistance and impaired insulin secretion, leading to hyperglycemia and hyperlipidemia. In addition to genetic factors, overnutrition is a major factor that results in the dysregulation of glucose homeostasis, contributing to the development of T2DM. Therefore, it is important to investigate the effect of nutritional regulation on glucose homeostasis and the underlying molecular mechanisms, thereby providing strategies for the prevention and treatment of T2DM. This Special Issue focuses on the impacts of nutrients on the control of glucose homeostasis and understanding their underlying mechanisms through hormone regulation, epigenetic modifications, gene transcriptional regulation, and chronic inflammation.

Dr. Shaodong Guo
Dr. Wanbao Yang
Guest Editors

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Keywords

type 2 diabetes
insulin resistance
nutrition
glucose homeostasis
hormone
epigenetic modification
chronic inflammation

Published Papers (3 papers)

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Research

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22 pages, 3025 KiB

Open AccessArticle

GHSR Deletion in β-Cells of Male Mice: Ineffective in Obesity, but Effective in Protecting against Streptozotocin-Induced β-Cell Injury in Aging

by Hye Won Han, Geetali Pradhan, Daniel Villarreal, Da Mi Kim, Abhishek Jain, Akhilesh Gaharwar, Yanan Tian, Shaodong Guo and Yuxiang Sun

Nutrients 2024, 16(10), 1464; https://doi.org/10.3390/nu16101464 - 13 May 2024

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Abstract

Insulin secretion from pancreatic β cells is a key pillar of glucose homeostasis, which is impaired under obesity and aging. Growth hormone secretagogue receptor (GHSR) is the receptor of nutrient-sensing hormone ghrelin. Previously, we showed that β-cell GHSR regulated glucose-stimulated insulin secretion (GSIS) in young mice. In the current study, we further investigated the effects of GHSR on insulin secretion in male mice under diet-induced obesity (DIO) and streptozotocin (STZ)-induced β-cell injury in aging. β-cell-specific-Ghsr-deficient (Ghsr-βKO) mice exhibited no glycemic phenotype under DIO but showed significantly improved ex vivo GSIS in aging. We also detected reduced insulin sensitivity and impaired insulin secretion during aging both in vivo and ex vivo. Accordingly, there were age-related alterations in expression of glucose transporter, insulin signaling pathway, and inflammatory genes. To further determine whether GHSR deficiency affected β-cell susceptibility to acute injury, young, middle-aged, and old Ghsr-βKO mice were subjected to STZ. We found that middle-aged and old Ghsr-βKO mice were protected from STZ-induced hyperglycemia and impaired insulin secretion, correlated with increased expression of insulin signaling regulators but decreased pro-inflammatory cytokines in pancreatic islets. Collectively, our findings indicate that β-cell GHSR has a major impact on insulin secretion in aging but not obesity, and GHSR deficiency protects against STZ-induced β-cell injury in aging. Full article

(This article belongs to the Special Issue Impact of Nutritional Regulation on the Control of Glucose Homeostasis and Type 2 Diabetes Mellitus)

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18 pages, 1713 KiB

Open AccessArticle

Effects of Quinine on the Glycaemic Response to, and Gastric Emptying of, a Mixed-Nutrient Drink in Females and Males

by Peyman Rezaie, Vida Bitarafan, Braden David Rose, Kylie Lange, Zinat Mohammadpour, Jens Frederik Rehfeld, Michael Horowitz and Christine Feinle-Bisset

Nutrients 2023, 15(16), 3584; https://doi.org/10.3390/nu15163584 - 15 Aug 2023

Cited by 2 | Viewed by 1225

Abstract

Intraduodenal quinine, in the dose of 600 mg, stimulates glucagon-like peptide-1 (GLP-1), cholecystokinin and insulin; slows gastric emptying (GE); and lowers post-meal glucose in men. Oral sensitivity to bitter substances may be greater in women than men. We, accordingly, evaluated the dose-related effects of quinine on GE, and the glycaemic responses to, a mixed-nutrient drink in females, and compared the effects of the higher dose with those in males. A total of 13 female and 13 male healthy volunteers received quinine-hydrochloride (600 mg (‘QHCl-600’) or 300 mg (‘QHCl-300’, females only) or control (‘C’), intraduodenally (10 mL bolus) 30 min before a drink (500 kcal, 74 g carbohydrates). Plasma glucose, insulin, C-peptide, GLP-1, glucose-dependent insulinotropic polypeptide (GIP) and cholecystokinin were measured at baseline, for 30 min after quinine alone, and then for 2 h post-drink. GE was measured by ¹³C-acetate breath-test. QHCl-600 alone stimulated insulin, C-peptide and GLP-1 secretion compared to C. Post-drink, QHCl-600 reduced plasma glucose, stimulated C-peptide and GLP-1, and increased the C-peptide/glucose ratio and oral disposition index, while cholecystokinin and GIP were less, in females and males. QHCl-600 also slowed GE compared to C in males and compared to QHCl-300 in females (p < 0.05). QHCl-300 reduced post-meal glucose concentrations and increased the C-peptide/glucose ratio, compared to C (p < 0.05). Magnitudes of glucose lowering and increase in C-peptide/glucose ratio by QHCl-600 were greater in females than males (p < 0.05). We conclude that quinine modulates glucoregulatory functions, associated with glucose lowering in healthy males and females. However, glucose lowering appears to be greater in females than males, without apparent differential effects on GI functions. Full article

(This article belongs to the Special Issue Impact of Nutritional Regulation on the Control of Glucose Homeostasis and Type 2 Diabetes Mellitus)

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Review

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23 pages, 2284 KiB

Open AccessReview

Regulation of Macronutrients in Insulin Resistance and Glucose Homeostasis during Type 2 Diabetes Mellitus

by Wanbao Yang, Wen Jiang and Shaodong Guo

Nutrients 2023, 15(21), 4671; https://doi.org/10.3390/nu15214671 - 4 Nov 2023

Cited by 5 | Viewed by 3694

Abstract

Insulin resistance is an important feature of metabolic syndrome and a precursor of type 2 diabetes mellitus (T2DM). Overnutrition-induced obesity is a major risk factor for the development of insulin resistance and T2DM. The intake of macronutrients plays a key role in maintaining energy balance. The components of macronutrients distinctly regulate insulin sensitivity and glucose homeostasis. Precisely adjusting the beneficial food compound intake is important for the prevention of insulin resistance and T2DM. Here, we reviewed the effects of different components of macronutrients on insulin sensitivity and their underlying mechanisms, including fructose, dietary fiber, saturated and unsaturated fatty acids, and amino acids. Understanding the diet-gene interaction will help us to better uncover the molecular mechanisms of T2DM and promote the application of precision nutrition in practice by integrating multi-omics analysis. Full article

(This article belongs to the Special Issue Impact of Nutritional Regulation on the Control of Glucose Homeostasis and Type 2 Diabetes Mellitus)

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