scholarly journals Soya protein reverses dyslipidaemia and the altered capacity of insulin-stimulated glucose utilization in the skeletal muscle of sucrose-rich diet-fed rats

2008 ◽  
Vol 102 (1) ◽  
pp. 60-68 ◽  
Author(s):  
María E. Oliva ◽  
Adriana G. Chicco ◽  
Yolanda B. Lombardo
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Homeostasis ◽  
Glucose Utilization ◽  
Body Weight Gain ◽  
Protein Isolate ◽  
Soya Protein ◽  
Whole Body ◽  
Control Group ◽  
Soya Protein Isolate

The present study investigates the benefits of dietary intake of soya protein upon dyslipidaemia and insulin resistance in rats chronically (8 months) fed a sucrose-rich (63 %) diet (SRD). For this purpose, we analysed the effectiveness of soya protein isolate in improving or reversing these metabolic abnormalities. Wistar rats were fed a SRD for 4 months. By the end of this period, stable dyslipidaemia and insulin resistance were present in the animals. From months 4 to 8, half the animals continued with the SRD and the other half were fed a SRD in which the source of protein casein was substituted by soya. The control group received a diet in which the source of carbohydrate was maize starch. The results showed that: (1) soya protein normalized plasma TAG, cholesterol and NEFA levels in the SRD-fed rats. Moreover, the addition of soya protein reversed the hepatic steatosis. (2) Glucose homeostasis was normalized without changes in circulating insulin levels. Whole-body peripheral insulin sensitivity substantially improved. Besides, soya protein moderately decreases body weight gain limiting the accretion of visceral fat. (3) By shifting the source of dietary protein from casein to soya during the last 4 months of the feeding period it was possible to reverse both the diminished insulin-stimulated glucose oxidation and disposal in the skeletal muscle of SRD-fed rats. This study provides new data showing the beneficial effect of soya protein upon lipid and glucose homeostasis in the experimental model of dyslipidaemia and insulin resistance.

Antioxidant supplemention in the treatment of skeletal muscle insulin resistance: potential mechanisms and clinical relevance

2008 ◽  
Vol 33 (1) ◽  
pp. 21-31 ◽  
Author(s):  
David Wright ◽  
Lindsey Sutherland
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Glucose Homeostasis ◽  
Whole Body ◽  
Antioxidant Compounds ◽  
Muscle Insulin Resistance ◽  
Beneficial Effects ◽  
Skeletal Muscle Insulin Resistance

The incidence of type 2 diabetes has increased dramatically over the past several decades and this trend is projected to continue into the foreseeable future. Skeletal muscle insulin resistance is thought to be a key development in the pathogenesis of type 2 diabetes. Given this fact, interventions that prevent or reverse impairments in skeletal muscle action can have profound effects on whole-body glucose homeostasis. Traditional approaches used in this regard include exercise, weight loss, and insulin-sensitizing drugs such as thiazolidinediones (TZDs). Although these interventions have proven effective in improving glucose homeostasis, there are adherence issues seen with lifestyle interventions and undesirable side effects have been reported with TZDs. With these points in mind, the development of alternative strategies to maintain or improve skeletal muscle insulin sensitivity is warranted. In this context, the purpose of the present review is to highlight the role of antioxidant compounds in the prevention and treatment of skeletal muscle insulin resistance. Specifically, we will briefly describe the mechanisms of insulin-stimulated skeletal muscle glucose uptake and the potential mediators of oxidative stress induced insulin resistance, highlight data suggesting that antioxidant compounds can have beneficial effects on skeletal muscle insulin action, and discuss potential mechanisms mediating this effect.

scholarly journals Removal of Epididymal Visceral Adipose Tissue Prevents Obesity-Induced Multi-organ Insulin Resistance in Male Mice

2021 ◽  
Vol 5 (5) ◽  
Author(s):  
Michael P Franczyk ◽  
Mai He ◽  
Jun Yoshino
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Visceral Adipose Tissue ◽  
Body Weight Gain ◽  
Whole Body ◽  
Atherogenic Dyslipidemia ◽  
Glucose And Lipid Metabolism ◽  
Visceral Adipose

Abstract Obesity is associated with insulin resistance, an important risk factor of type 2 diabetes, atherogenic dyslipidemia, and nonalcoholic fatty liver disease. The major purpose of this study was to test hypothesize that prophylactic removal of epididymal visceral adipose tissue (VAT) prevents obesity-induced multi-organ (liver, skeletal muscle, adipose tissue) insulin resistance. Accordingly, we surgically removed epididymal VAT pads from adult C57BL/6J mice and evaluated in vivo and cellular metabolic pathways involved in glucose and lipid metabolism following chronic high-fat diet (HFD) feeding. We found that VAT removal decreases HFD-induced body weight gain while increasing subcutaneous adipose tissue (SAT) mass. Strikingly, VAT removal prevents obesity-induced insulin resistance and hyperinsulinemia and markedly enhances insulin-stimulated AKT-phosphorylation at serine-473 (Ser473) and threonine-308 (Thr308) sites in SAT, liver, and skeletal muscle. VAT removal leads to decreases in plasma lipid concentrations and hepatic triglyceride (TG) content. In addition, VAT removal increases circulating adiponectin, a key insulin-sensitizing adipokine, whereas it decreases circulating interleukin 6, a pro-inflammatory adipokine. Consistent with these findings, VAT removal increases adenosine monophosphate–activated protein kinase C phosphorylation, a major downstream target of adiponectin signaling. Data obtained from RNA sequencing suggest that VAT removal prevents obesity-induced oxidative stress and inflammation in liver and SAT, respectively. Taken together, these findings highlight the metabolic benefits and possible action mechanisms of prophylactic VAT removal on obesity-induced insulin resistance and hepatosteatosis. Our results also provide important insight into understanding the extraordinary capability of adipose tissue to influence whole-body glucose and lipid metabolism as an active endocrine organ.

scholarly journals Perioperative Infusion of Glucagon-Like Peptide-1 Prevents Insulin Resistance After Surgical Trauma in Female Pigs

Endocrinology ◽  
2019 ◽  
Vol 160 (12) ◽  
pp. 2892-2902
Author(s):  
Martin Hagve ◽  
Petter F Gjessing ◽  
Mikal J Hole ◽  
Kirsten M Jansen ◽  
Ole Martin Fuskevåg ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Whole Body ◽  
Glucose Disposal ◽  
Control Group ◽  
Surgical Trauma ◽  
Glucose Release ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Abstract Insulin resistance is an independent negative predictor of outcome after elective surgery and increases mortality among surgical patients in intensive care. The incretin hormone glucagon-like peptide-1 (GLP-1) potentiates glucose-induced insulin release from the pancreas but may also increase insulin sensitivity in skeletal muscle and directly suppress hepatic glucose release. Here, we investigated whether a perioperative infusion of GLP-1 could counteract the development of insulin resistance after surgery. Pigs were randomly assigned to three groups; surgery/control, surgery/GLP-1, and sham/GLP-1. Both surgery groups underwent major abdominal surgery. Whole-body glucose disposal (WGD) and endogenous glucose release (EGR) were assessed preoperatively and postoperatively using D-[6,6-2H2]-glucose infusion in combination with hyperinsulinemic euglycemic step-clamping. In the surgery/control group, peripheral insulin sensitivity (i.e., WGD) was reduced by 44% relative to preoperative conditions, whereas the corresponding decline was only 9% for surgery/GLP-1 (P < 0.05). Hepatic insulin sensitivity (i.e., EGR) remained unchanged in the surgery/control group but was enhanced after GLP-1 infusion in both surgery and sham animals (40% and 104%, respectively, both P < 0.05). Intraoperative plasma glucose increased in surgery/control (∼20%) but remained unchanged in both groups receiving GLP-1 (P < 0.05). GLP-1 diminished an increase in postoperative glucagon levels but did not affect skeletal muscle glycogen or insulin signaling proteins after surgery. We show that GLP-1 improves intraoperative glycemic control, diminishes peripheral insulin resistance after surgery, and suppresses EGR. This study supports the use of GLP-1 to prevent development of postoperative insulin resistance.

Selective activation of PPARγ in skeletal muscle induces endogenous production of adiponectin and protects mice from diet-induced insulin resistance

2010 ◽  
Vol 298 (1) ◽  
pp. E28-E37 ◽  
Author(s):  
Rajesh H. Amin ◽  
Suresh T. Mathews ◽  
Heidi S. Camp ◽  
Liyun Ding ◽  
Todd Leff
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Transgenic Mice ◽  
Muscle Tissue ◽  
Glucose Homeostasis ◽  
Muscle Cells ◽  
Whole Body ◽  
Fiber Types ◽  
Dependent Manner

The nuclear receptor peroxisome proliferator-activated receptor (PPAR)γ plays a key role in regulating whole body glucose homeostasis and insulin sensitivity. Although it is expressed most highly in adipose, it is also present at lower levels in many tissues, including skeletal muscle. The role muscle PPARγ plays in metabolic regulation and in mediating the antidiabetic effects of the thiazolidinediones is not understood. The goal of this work was to examine the molecular and physiological effects of PPARγ activation in muscle cells. We found that pharmacological activation of PPARγ in primary cultured myocytes, and genetic activation of muscle PPARγ in muscle tissue of transgenic mice, induced the production of adiponectin directly from muscle cells. This muscle-produced adiponectin was functional and capable of stimulating adiponectin signaling in myocytes. In addition, elevated skeletal muscle PPARγ activity in transgenic mice provided a significant protection from high-fat diet-induced insulin resistance and associated changes in muscle phenotype, including reduced myocyte lipid content and an increase in the proportion of oxidative muscle fiber types. Our findings demonstrate that PPARγ activation in skeletal muscle can have a significant protective effect on whole body glucose homeostasis and insulin resistance and that myocytes can produce and secrete functional adiponectin in a PPARγ-dependent manner. We propose that activation of PPARγ in myocytes induces a local production of adiponectin that acts on muscle tissue to improve insulin sensitivity.

Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism

2007 ◽  
Vol 292 (3) ◽  
pp. E654-E667 ◽  
Author(s):  
Dake Qi ◽  
Brian Rodrigues
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Glucose Utilization ◽  
Experimental Studies ◽  
Cardiac Metabolism ◽  
Multiple Organ ◽  
Whole Body ◽  
Metabolic Abnormalities ◽  
Organ Systems ◽  
Per Se

Insulin resistance is viewed as an insufficiency in insulin action, with glucocorticoids being recognized to play a key role in its pathogenesis. With insulin resistance, metabolism in multiple organ systems such as skeletal muscle, liver, and adipose tissue is altered. These metabolic alterations are widely believed to be important factors in the morbidity and mortality of cardiovascular disease. More importantly, clinical and experimental studies have established that metabolic abnormalities in the heart per se also play a crucial role in the development of heart failure. Following glucocorticoids, glucose utilization is compromised in the heart. This attenuated glucose metabolism is associated with altered fatty acid supply, composition, and utilization. In the heart, elevated fatty acid use has been implicated in a number of metabolic, morphological, and mechanical changes and, more recently, in “lipotoxicity”. In the present article, we review the action of glucocorticoids, their role in insulin resistance, and their influence in modulating peripheral and cardiac metabolism and heart disease.

scholarly journals Tail suspension is useful as a sarcopenia model in rats

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Akira Nemoto ◽  
Toru Goyagi
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Experimental Model ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Whole Body ◽  
Skeletal Muscle Atrophy ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Simple Method

Abstract Background Sarcopenia promotes skeletal muscle atrophy and exhibits a high mortality rate. Its elucidation is of the highest clinical importance, but an animal experimental model remains controversial. In this study, we investigated a simple method for studying sarcopenia in rats. Results Muscle atrophy was investigated in 24-week-old, male, tail-suspended (TS), Sprague Dawley and spontaneously hypertensive rats (SHR). Age-matched SD rats were used as a control group. The skeletal muscle mass weight, muscle contraction, whole body tension (WBT), cross-sectional area (CSA), and Muscle RING finger-1 (MuRF-1) were assessed. Enzyme-linked immunosorbent assay was used to evaluate the MuRF-1 levels. Two muscles, the extensor digitorum longus and soleus muscles, were selected for representing fast and slow muscles, respectively. All data, except CSA, were analyzed by a one-way analysis of variance, whereas CSA was analyzed using the Kruskal-Wallis test. Muscle mass weight, muscle contraction, WBT, and CSA were significantly lower in the SHR (n = 7) and TS (n = 7) groups than in the control group, whereas MuRF-1 expression was dominant. Conclusions TS and SHR presented sarcopenic phenotypes in terms of muscle mass, muscle contraction and CSA. TS is a useful technique for providing muscle mass atrophy and weakness in an experimental model of sarcopenia in rats.

scholarly journals Hepatokine ERAP1 impairs skeletal muscle insulin sensitivity via ADRB2/PKA pathway

2020 ◽  
Author(s):  
Feifan Guo ◽  
Yuguo Niu ◽  
Haizhou Jiang ◽  
Hanrui Yin ◽  
Fenfen Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Neutralizing Antibodies ◽  
Leptin Receptor ◽  
Whole Body ◽  
C2c12 Myotubes ◽  
Insulin Resistant ◽  
Skeletal Muscle Insulin Sensitivity ◽  
Pka Pathway

Abstract The current study aimed to investigate the role of endoplasmic reticulum aminopeptidase 1 (ERAP1), a novel hepatokine, in whole-body glucose metabolism. Here, we found that hepatic ERAP1 levels were increased in insulin-resistant leptin-receptor-mutated (db/db) and high-fat diet (HFD)-fed mice. Consistently, hepatic ERAP1 overexpression attenuated skeletal muscle (SM) insulin sensitivity, whereas knockdown ameliorated SM insulin resistance. Furthermore, serum and hepatic ERAP1 levels were positively correlated, and recombinant mouse ERAP1 or conditioned medium with high ERAP1 content (CM-ERAP1) attenuated insulin signaling in C2C12 myotubes, and CM-ERAP1 or HFD-induced insulin resistance was blocked by ERAP1 neutralizing antibodies. Mechanistically, ERAP1 reduced ADRB2 expression and interrupted ADRB2-dependent signaling in C2C12 myotubes. Finally, ERAP1 inhibition via global knockout or the inhibitor thimerosal improved insulin sensitivity. Together, ERAP1 is a hepatokine that impairs SM and whole-body insulin sensitivity, and its inhibition might provide a therapeutic strategy for diabetes, particularly for those with SM insulin resistance.

scholarly journals Hepatic glucose utilization in hepatic steatosis and obesity

2016 ◽  
Vol 36 (6) ◽  
Author(s):  
Georgia Keramida ◽  
James Hunter ◽  
Adrien Michael Peters
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Glucose Utilization ◽  
Graphical Analysis ◽  
Whole Body ◽  
Utilization Rate ◽  
Obese Patients ◽  
Pet Ct ◽  
Significant Difference ◽  
Hepatic Glucose

Hepatic steatosis is associated with obesity and insulin resistance. Whether hepatic glucose utilization rate (glucose phosphorylation rate; MRglu) is increased in steatosis and/or obesity is uncertain. Our aim was to determine the separate relationships of steatosis and obesity with MRglu. Sixty patients referred for routine PET/CT had dynamic PET imaging over the abdomen for 30 min post-injection of F-18-fluorodeoxyglucose (FDG), followed by Patlak–Rutland graphical analysis of the liver using abdominal aorta for arterial input signal. The plot gradient was divided by the intercept to give hepatic FDG clearance normalized to hepatic FDG distribution volume (ml/min per 100 ml) and multiplied by blood glucose to give hepatic MRglu (μmol/min per 100 ml). Hepatic steatosis was defined as CT density of ≤40 HU measured from the 60 min whole body routine PET/CT and obesity as body mass index of ≥30 kg/m2. Hepatic MRglu was higher in patients with steatosis (3.3±1.3 μmol/min per 100 ml) than those without (1.7±1.2 μmol/min per 100 ml; P<0.001) but there was no significant difference between obese (2.5±1.6 μmol/min per 100 ml) and non-obese patients (2.1±1.3 μmol/min per 100 ml). MRglu was increased in obese patients only if they had steatosis. Non-obese patients with steatosis still had increased MRglu. There was no association between MRglu and chemotherapy history. We conclude that MRglu is increased in hepatic steatosis probably through insulin resistance, hyperinsulinaemia and up-regulation of hepatic hexokinase, irrespective of obesity.

Sign in / Sign up

Export Citation Format

Share Document