scholarly journals Exercise Affects Blood Glucose Levels and Tissue Chromium Distribution in High-Fat Diet-Fed C57BL6 Mice

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1658 ◽  
Author(s):  
Geng-Ruei Chang ◽  
Po-Hsun Hou ◽  
Wen-Kai Chen ◽  
Chien-Teng Lin ◽  
Hsiao-Pei Tsai ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
High Fat Diet ◽  
Cell Function ◽  
Body Weight Gain ◽  
Liver Fat ◽  
Standard Diet ◽  
Model Assessment ◽  
Obese Mice ◽  
High Fat

Obesity is commonly associated with hyperglycemia and type 2 diabetes and negatively affects chromium accumulation in tissues. Exercise prevents and controls obesity and type 2 diabetes. However, little information is available regarding chromium changes for regulating glucose homeostasis in high-fat diet (HFD)-fed animals/humans who exercise. Therefore, this study explored the effects of exercise and whether it alters chromium distribution in obese mice. Male C57BL6/J mice aged 4 weeks were randomly divided into two groups and fed either an HFD or standard diet (SD). Each group was subgrouped into two additional groups in which one subgroup was exposed to treadmill exercise for 12 weeks and the other comprised control mice. HFD-fed mice that exercised exhibited significant lower body weight gain, food/energy intake, daily food efficiency, and serum leptin and insulin levels than did HFD-fed control mice. Moreover, exercise reduced fasting glucose and enhanced insulin sensitivity and pancreatic β-cell function, as determined by homeostasis model assessment (HOMA)-insulin resistance and HOMA-β indices, respectively. Exercise also resulted in markedly higher chromium levels within the muscle, liver, fat tissues, and kidney but lower chromium levels in the bone and bloodstream in obese mice than in control mice. However, these changes were not noteworthy in SD-fed mice that exercised. Thus, exercise prevents and controls HFD-induced obesity and may modulate chromium distribution in insulin target tissues.

scholarly journals Tetrahydrocurcumin Upregulates the Adiponectin-AdipoR Pathway and Improves Insulin Signaling and Pancreatic β-Cell Function in High-Fat Diet/Streptozotocin-Induced Diabetic Obese Mice

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4552
Author(s):  
Yi-Zhen Tsai ◽  
Mei-Ling Tsai ◽  
Li-Yin Hsu ◽  
Chi-Tang Ho ◽  
Ching-Shu Lai
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Signaling ◽  
High Fat Diet ◽  
Cell Function ◽  
Obese Mice ◽  
High Fat ◽  
Islet Mass ◽  
Beneficial Effects ◽  
Β Cell Function

Impairment of adiponectin production and function is closely associated with insulin resistance and type 2 diabetes, which are linked to obesity. Studies in animal models have documented the anti-diabetic effects of tetrahydrocurcumin (THC). Although several possible mechanisms have been proposed, the contribution of adiponectin signaling on THC-mediated antihyperglycemic effects remains unknown. Here, we report that adiposity, steatosis, and hyperglycemia were potently attenuated in high-fat diet/streptozotocin-induced diabetic obese mice after they received 20 and 100 mg/kg THC for 14 weeks. THC upregulated UCP-1 in adipose tissue and elevated adiponectin levels in the circulation. THC upregulated the AdipoR1/R2-APPL1-mediated pathway in the liver and skeletal muscle, which contributes to improved insulin signaling, glucose utilization, and lipid metabolism. Furthermore, THC treatment significantly (p < 0.05) preserved islet mass, reduced apoptosis, and restored defective insulin expression in the pancreatic β-cells of diabetic obese mice, which was accompanied by an elevation of AdipoR1 and APPL1. These results demonstrated a potential mechanism underlying the beneficial effects of THC against hyperglycemia via the adiponectin-AdipoR pathway, and thus, may lead to a novel therapeutic use for type 2 diabetes.

scholarly journals Baicalein Protects against Type 2 Diabetes via Promoting Isletβ-Cell Function in Obese Diabetic Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Yu Fu ◽  
Jing Luo ◽  
Zhenquan Jia ◽  
Wei Zhen ◽  
Kequan Zhou ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Cell Function ◽  
Diabetic Mice ◽  
Obese Mice ◽  
High Fat ◽  
Middle Aged

In both type 1 (T1D) and type 2 diabetes (T2D), the deterioration of glycemic control over time is primarily caused by an inadequate mass and progressive dysfunction ofβ-cell, leading to the impaired insulin secretion. Here, we show that dietary supplementation of baicalein, a flavone isolated from the roots of Chinese herbScutellaria baicalensis, improved glucose tolerance and enhanced glucose-stimulated insulin secretion (GSIS) in high-fat diet (HFD-) induced middle-aged obese mice. Baicalein had no effect on food intake, body weight gain, circulating lipid profile, and insulin sensitivity in obese mice. Using another mouse model of type 2 diabetes generated by high-fat diet (HFD) feeding and low doses of streptozotocin injection, we found that baicalein treatment significantly improved hyperglycemia, glucose tolerance, and blood insulin levels in these middle-aged obese diabetic mice, which are associated with the improved isletβ-cell survival and mass. In thein vitrostudies, baicalein significantly augmented GSIS and promoted viability of insulin-secreting cells and human islets cultured either in the basal medium or under chronic hyperlipidemic condition. These results demonstrate that baicalein may be a naturally occurring antidiabetic agent by directly modulating pancreaticβ-cell function.

scholarly journals Leptin restores the insulinotropic effect of exenatide in a mouse model of type 2 diabetes with increased adiposity induced by streptozotocin and high-fat diet

2014 ◽  
Vol 307 (8) ◽  
pp. E712-E719 ◽  
Author(s):  
Takeru Sakai ◽  
Toru Kusakabe ◽  
Ken Ebihara ◽  
Daisuke Aotani ◽  
Sachiko Yamamoto-Kataoka ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Triglyceride Level ◽  
High Fat Diet ◽  
Receptor Agonist ◽  
Cell Function ◽  
High Fat ◽  
Β Cell ◽  
Β Cell Function ◽  
Insulinotropic Effect

Leptin may reduce pancreatic lipid deposition, which increases with progression of obesity and can impair β-cell function. The insulinotropic effect of glucagon-like peptide-1 (GLP-1) and the efficacy of GLP-1 receptor agonist are reduced associated with impaired β-cell function. In this study, we examined whether leptin could restore the efficacy of exenatide, a GLP-1 receptor agonist, in type 2 diabetes with increased adiposity. We chronically administered leptin (500 μg·kg−1·day−1) and/or exenatide (20 μg·kg−1·day−1) for 2 wk in a mouse model of type 2 diabetes with increased adiposity induced by streptozotocin and high-fat diet (STZ/HFD mice). The STZ/HFD mice exhibited hyperglycemia, overweight, increased pancreatic triglyceride level, and reduced glucose-stimulated insulin secretion (GSIS); moreover, the insulinotropic effect of exenatide was reduced. However, leptin significantly reduced pancreatic triglyceride level, and adding leptin to exenatide (LEP/EX) remarkably enhanced GSIS. These results suggested that the leptin treatment restored the insulinotropic effect of exenatide in the mice. In addition, LEP/EX reduced food intake, body weight, and triglyceride levels in the skeletal muscle and liver, and corrected hyperglycemia to a greater extent than either monotherapy. The pair-feeding experiment indicated that the marked reduction of pancreatic triglyceride level and enhancement of GSIS by LEP/EX occurred via mechanisms other than calorie restriction. These results suggest that leptin treatment may restore the insulinotropic effect of exenatide associated with the reduction of pancreatic lipid deposition in type 2 diabetes with increased adiposity. Combination therapy with leptin and exenatide could be an effective treatment for patients with type 2 diabetes with increased adiposity.

scholarly journals Polyphenol-Rich Fraction of Brown AlgaEcklonia cavaCollected from Gijang, Korea, Reduces Obesity and Glucose Levels in High-Fat Diet-Induced Obese Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Eun Young Park ◽  
Eung Hwi Kim ◽  
Mi Hwi Kim ◽  
Young Wan Seo ◽  
Jung Im Lee ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Body Weight ◽  
Glucose Tolerance ◽  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Glucose Levels

Ecklonia cava (E. cava)is a brown alga that has beneficial effects in models of type 1 and type 2 diabetes. However, the effects ofE. cavaextracts on diet-induced obesity and type 2 diabetes have not been specifically examined. We investigated the effects ofE. cavaon body weight, fat content, and hyperglycemia in high-fat diet- (HFD) induced obese mice and sought the mechanisms involved. C57BL/6 male mice were fed a HFD (60% fat) diet or normal chow. After 3 weeks, the HFD diet group was given extracts (200 mg/kg) ofE. cavaharvested from Jeju (CA) or Gijang (G-CA), Korea or PBS by oral intubation for 8 weeks. Body weights were measured weekly. Blood glucose and glucose tolerance were measured at 7 weeks, and fat pad content and mRNA expression of adipogenic genes and inflammatory cytokines were measured after 8 weeks of treatment. G-CA was effective in reducing body weight gain, body fat, and hyperglycemia and improving glucose tolerance as compared with PBS-HFD mice. The mRNA expression of adipogenic genes was increased, and mRNA expression of inflammatory cytokines and macrophage marker gene was decreased in G-CA-treated obese mice. We suggest that G-CA reduces obesity and glucose levels by anti-inflammatory actions and improvement of lipid metabolism.

scholarly journals High-fat diet-induced glucose dysregulation is independent of changes in islet ACE2 in mice

2016 ◽  
Vol 311 (6) ◽  
pp. R1223-R1233 ◽  
Author(s):  
Harshita Chodavarapu ◽  
Kavaljit H. Chhabra ◽  
Huijing Xia ◽  
Vinayak Shenoy ◽  
Xinping Yue ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Cell Function ◽  
Physiological Role ◽  
Experimental Models ◽  
Minor Role ◽  
Ang Ii ◽  
High Fat

While restoration of ACE2 activity in the pancreas leads to improvement of glycemia in experimental models of Type 2 diabetes, global deficiency in ACE2 disrupts β-cell function and impairs glucose tolerance in mice, demonstrating the physiological role of ACE2 in glucose homeostasis. Although the contribution of pancreatic ACE2 to glucose regulation has been demonstrated in genetic models of diabetes and in models with overexpression of the renin-angiotensin system (RAS), it is unclear whether islet ACE2 is involved in glycemic control in common models of human Type 2 diabetes. To determine whether diet-induced diabetes deregulates glucose homeostasis via reduction of ACE2 in the pancreatic islets, wild-type (WT) and ACE2 knockout (KO) male mice were fed a high-fat diet (HFD) for 16 wk. ACE2 KO mice were more susceptible than WT mice to HFD-mediated glycemic dysregulation. Islet ACE2 activity and expression of various genes, including ANG II type 1a receptor (mAT1aR) were then assessed. Surprisingly, we observed no change in islet ACE2 activity and expression despite local RAS overactivity, indicated by an upregulation of mAT1aR expression. Despite a predominant expression in islet α-cells, further investigation highlighted a minor role for ACE2 on glucagon expression. Further, pancreatic ACE2 gene therapy improved glycemia in HFD-fed WT mice, leading to enhanced glucose-stimulated insulin secretion, reduced pancreatic ANG II levels, fibrosis, and ADAM17 activity. Altogether, our study demonstrates that HFD feeding increases RAS activity and mediates glycemic dysregulation likely through loss of ACE2 present outside the islets but independently of changes in islet ACE2.

scholarly journals High-fat diet ingestion correlates with neuropathy in the duodenum myenteric plexus of obese mice with symptoms of type 2 diabetes

2013 ◽  
Vol 354 (2) ◽  
pp. 381-394 ◽  
Author(s):  
Chloe M. Stenkamp-Strahm ◽  
Adam J. Kappmeyer ◽  
Joe T. Schmalz ◽  
Martin Gericke ◽  
Onesmo Balemba
Keyword(s):  
Type 2 Diabetes ◽  
Myenteric Plexus ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat

scholarly journals The Antiinflammatory Cytokine Interleukin-1 Receptor Antagonist Protects from High-Fat Diet-Induced Hyperglycemia

Endocrinology ◽  
2008 ◽  
Vol 149 (5) ◽  
pp. 2208-2218 ◽  
Author(s):  
Nadine S. Sauter ◽  
Fabienne T. Schulthess ◽  
Ryan Galasso ◽  
Lawrence W. Castellani ◽  
Kathrin Maedler
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Receptor Antagonist ◽  
High Fat Diet ◽  
Cell Function ◽  
Interleukin 1 ◽  
High Fat ◽  
Β Cell

Subclinical inflammation is a recently discovered phenomenon in type 2 diabetes. Elevated cytokines impair β-cell function and survival. A recent clinical trial shows that blocking IL-1β signaling by IL-1 receptor antagonist (IL-1Ra) improves β-cell secretory function in patients with type 2 diabetes. In the present study, we provide further mechanisms of the protective role of IL-1Ra on the β-cell. IL-1Ra prevented diabetes in vivo in C57BL/6J mice fed a high-fat/high-sucrose diet (HFD) for 12 wk; it improved glucose tolerance and insulin secretion. High-fat diet treatment increased serum levels of free fatty acids and of the adipokines resistin and leptin, which were reduced by IL-1Ra treatment. In addition, IL-1Ra counteracted adiponectin levels, which were decreased by high-fat feeding. Studies on isolated islets revealed that IL-1Ra specifically acted on the β-cell. IL-1Ra protected islets from HFD treated animals from β-cell apoptosis, induced β-cell proliferation, and improved glucose-stimulated insulin secretion. Insulin mRNA was reduced in islets from mice fed a HFD but normalized in the IL-1Ra group. Our results show that IL-1Ra improves β-cell survival and function, and support the potential role for IL-1Ra in the treatment of diabetes.

scholarly journals Modulatory Effect of Polyphenolic Compounds from the Mangrove Tree Rhizophora mangle L. on Non-Alcoholic Fatty Liver Disease and Insulin Resistance in High-Fat Diet Obese Mice

Molecules ◽  
2018 ◽  
Vol 23 (9) ◽  
pp. 2114 ◽  
Author(s):  
Leonardo de Souza Mesquita ◽  
Cíntia Caria ◽  
Paola Santos ◽  
Caio Ruy ◽  
Natalia da Silva Lima ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Rhizophora Mangle ◽  
Mrna Levels ◽  
Obese Mice ◽  
High Fat ◽  
Mangrove Tree

No scientific report proves the action of the phytochemicals from the mangrove tree Rhizophora mangle in the treatment of diabetes. The aim of this work is to evaluate the effects of the acetonic extract of R. mangle barks (AERM) on type 2 diabetes. The main chemical constituents of the extract were analyzed by high-performance liquid chromatography (HPLC) and flow injection analysis electrospray-iontrap mass spectrometry (FIA-ESI-IT-MS/MS). High-fat diet (HFD)-fed mice were used as model of type 2 diabetes associated with obesity. After 4 weeks of AERM 5 or 50 mg/kg/day orally, glucose homeostasis was evaluated by insulin tolerance test (kiTT). Hepatic steatosis, triglycerides and gene expression were also evaluated. AERM consists of catechin, quercetin and chlorogenic acids derivatives. These metabolites have nutritional importance, obese mice treated with AERM (50 mg/kg) presented improvements in insulin resistance resulting in hepatic steatosis reductions associated with a strong inhibition of hepatic mRNA levels of CD36. The beneficial effects of AERM in an obesity model could be associated with its inhibitory α-amylase activity detected in vitro. Rhizophora mangle partially reverses insulin resistance and hepatic steatosis associated with obesity, supporting previous claims in traditional knowledge.

scholarly journals Anti-Obesity Effects of Sargassum thunbergii via Downregulation of Adipogenesis Gene and Upregulation of Thermogenic Genes in High-Fat Diet-Induced Obese Mice

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3325
Author(s):  
Min-Cheol Kang ◽  
Hyo-Geun Lee ◽  
Hyun-Soo Kim ◽  
Kyung-Mo Song ◽  
Yong-Gi Chun ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Sargassum Thunbergii ◽  
Fat Accumulation

Obesity is a metabolic disease characterized by an increased risk of type 2 diabetes, hypertension, and cardiovascular disease. We have previously reported that compounds isolated from brown alga, Sargassum thunbergii (ST; Sargassum thunbergii (Mertens ex Roth) Kuntze), inhibit adipogenesis in 3T3-L1 cells. However, the in vivo anti-obesity effects of these compounds have not been previously reported. Therefore, the objective of this study was to determine the effects of ST on weight loss, fat accumulation, as well as risk factors for type 2 diabetes and cardiovascular disease in high-fat diet (HFD)-induced obese mice. ST treatment significantly decreased body weight and fat accumulation in HFD-induced obese mice, while reducing insulin and factors related to cardiovascular diseases (triglyceride and total cholesterol) in serum. ST-induced downregulation of PPARγ in white adipose tissue, and upregulation of the thermogenic genes, UCP-1 and UCP-3, in brown adipose tissue was also observed. In addition, oral administration of ST reduced the occurrence of fatty liver, as well as the amount of white adipose tissue in HFD mice. Cumulatively, these results suggest that ST exerts anti-obesity effects and may serve as a potential anti-obesity therapeutic agent.

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