scholarly journals Increased Energy Expenditure and Energy Loss through Feces Contribute to the Long-term Outcome of Roux-en-Y Gastric Bypass on Diet Induced Obese Mouse Model

2020 ◽  
Author(s):  
Kai Chen ◽  
Boen Xiao ◽  
Zhe Zhou ◽  
Weihui Peng ◽  
wei liu
Keyword(s):  
Body Weight ◽  
Energy Metabolism ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Sham Group ◽  
Tolerance Test ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Insulin Tolerance

Abstract Background Roux-en-Y gastric bypass (RYGB) has been proved to be more effective than other bariatric procedures in long-term on body weight loss and remission of diabetes. However, the mechanism remains poorly understood. Long-term change of energy metabolism after RYGB has rarely been reported. Objectives To investigate the long-term outcome of RYGB on mouse model and its mechanism from the perspective of energy metabolism. Methods High-fat diet induced obesity (DIO) mice were assigned to two groups receiving RYGB(n=8) and sham operation(n=7), followed by high-fat diet feeding until 12 weeks after surgery. Body weight and food intake were recorded weekly, measurement of body composition and energy metabolism by metabolic chamber were conducted on week 4, 8 and 12 after surgery. Fecal energy measurement, Intraperitoneal Glucose Tolerance Test (IPGTT) and Insulin Tolerance Test (ITT) were conducted on week 12 after surgery.Results Food intake was reduced in RYGB group within the first 3 weeks after surgery and increased to be the same withSham group from postoperative week 4. At 12 weeks after surgery, body weight reduced by 36±3.2% in RYGB group comparing to 16±2% body weight gain in Sham group, while fat mass was significantly reduced in RYGB group than in Sham group (9.2±1.5% versus 30.1±0.7%). Energy expenditure was significantly higher on postoperative week 8 in RYGB group than in Sham group. In comparison with Sham group, respiratory exchange ratio (RER) was unchanged, decreased and increased in RYGB group at postoperative week 4, 8 and 12, respectively. Fecal energy measurementshowed that feces from mice in RYGB group contained higher energy level than Sham group. Glucose metabolism was significantly improved in RYGB group in contrast to Sham group, demonstrated by the result of Intraperitoneal Glucose Tolerance Test (IPGTT) (AUC: 1502± 104 versus 2277±198, respectively) and the Insulin Tolerance Test (ITT) (AUC: 524 ±50 versus 838±63, respectively). Conclusions Increased energy expenditure and energy loss through feces contribute to the long-term body weight control after RYGB. Enhanced glucose utilization might play a role in the long-term improvement of glucose metabolism.

α1-Antitrypsin A treatment attenuates neutrophil elastase accumulation and enhances insulin sensitivity in adipose tissue of mice fed a high-fat diet.

2021 ◽  
Author(s):  
Randall F. D'Souza ◽  
Stewart W.C. Masson ◽  
Jonathan S. T. Woodhead ◽  
Samuel L James ◽  
Caitlin MacRae ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Neutrophil Elastase ◽  
High Fat Diet ◽  
Tolerance Test ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Insulin Tolerance

Neutrophils accumulate in insulin sensitive tissues during obesity and may play a role in impairing insulin sensitivity. The major serine protease expressed by neutrophils is neutrophil elastase (NE), which is inhibited endogenously by α1-antitrypsin A (A1AT). We investigated the effect of exogenous (A1AT) treatment on diet induced metabolic dysfunction. Male C57Bl/6j mice fed a chow or a high fat diet (HFD) were randomized to receive 3x weekly i.p injections of either Prolastin (human A1AT; 2mg) or vehicle (PBS) for 10 weeks. Prolastin treatment did not affect plasma NE concentration, body weight, glucose tolerance or insulin sensitivity in chow fed mice. In contrast, Prolastin treatment attenuated HFD induced increases in plasma and white adipose tissue (WAT) NE without affecting circulatory neutrophil levels or increases in body weight. Prolastin-treated mice fed a HFD had improved insulin sensitivity, as assessed by insulin tolerance test, and this was associated with higher insulin-dependent IRS-1 (insulin receptor substrate) and AktSer473phosphorylation, and reduced inflammation markers in WAT but not liver or muscle. In 3T3-L1 adipocytes, Prolastin reversed recombinant NE-induced impairment of insulin-stimulated glucose uptake and IRS-1 phosphorylation. Furthermore, PDGF mediated p-AktSer473 activation and glucose uptake (which is independent of IRS-1) was not affected by recombinant NE treatment. Collectively, our findings suggest that NE infiltration of WAT during metabolic overload contributes to insulin-resistance by impairing insulin-induced IRS-1 signaling.

scholarly journals Effect of Forskolin on Body Weight, Glucose Metabolism and Adipocyte Size of Diet-Induced Obesity in Mice

Animals ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 645
Author(s):  
Jing-Yi Chen ◽  
Shao-Yu Peng ◽  
Yeong-Hsiang Cheng ◽  
I-Ta Lee ◽  
Yu-Hsiang Yu
Keyword(s):  
Body Weight ◽  
Glucose Metabolism ◽  
Dimethyl Sulfoxide ◽  
High Fat Diet ◽  
Tolerance Test ◽  
Cell Diameter ◽  
High Fat ◽  
Fat Cell ◽  
Glucose Levels ◽  
Insulin Tolerance

The purpose of this study was to investigate the effects of forskolin on body weight, glucose metabolism and fat cell diameter in high-fat diet-induced obese mice. Four-week-old male mice (C57BL/6) were randomly assigned to 1 of 3 treatment groups: a high-fat diet plus 5% dimethyl sulfoxide (vehicle), high-fat diet plus 2 mg/kg of forskolin (dissolved in 5% dimethyl sulfoxide) and high-fat diet plus 4 mg/kg of forskolin (dissolved in 5% dimethyl sulfoxide). Forskolin or dimethyl sulfoxide was administered intraperitoneally every two days. The results indicated that no significant difference was observed in the body weight, feed intake and serum lipid parameters among groups at 20 weeks of age. The blood glucose levels were significantly reduced in the groups treated with 2 mg/kg of forskolin before glucose tolerance test. Forskolin administration linearly decreased blood glucose levels of high-fat diet-fed mice at 90 min and total area under curve (AUC) after insulin tolerance test. The subcutaneous adipocyte diameter was significantly reduced in the groups treated with 2 mg/kg of forskolin. Forskolin administration linearly reduced the gonadal adipocyte diameter of high-fat diet-fed mice. Forskolin significantly reduced the differentiation of murine mesenchymal stem cells into adipocytes and this was accompanied by a decrease in intracellular triglyceride content and an increase in glycerol concentration in the culture medium. The subcutaneous adipocyte diameter, gonadal adipocyte diameter and total AUC of insulin tolerance test were moderately negatively correlated with the concentration of forskolin in the high-fat diet-induced obese model. These results demonstrate that forskolin can regulate glucose metabolism and reduce fat cell diameter of high-fat diet-fed mice and inhibit the adipocyte differentiation of murine mesenchymal stem cells.

EFFECT OF THE KIDNEY WEIGHT/BODY WEIGHT (Kw/Bw) RATIO IN THE LONG-TERM OUTCOME OF LIVING KIDNEY TRANSPLANTATION.

1999 ◽  
Vol 67 (7) ◽  
pp. S88
Author(s):  
Kazunari Tanabe ◽  
Tadahiko Tokumoto ◽  
Nobuo Ishikawa ◽  
Tomokazu Shimizu ◽  
Hiroaki Shinmura ◽  
...  
Keyword(s):  
Body Weight ◽  
Kidney Transplantation ◽  
Kidney Weight ◽  
Term Outcome ◽  
Long Term Outcome

Long-term metabolic benefits of exenatide in mice are mediated solely via the known glucagon-like peptide 1 receptor

2014 ◽  
Vol 306 (7) ◽  
pp. R490-R498 ◽  
Author(s):  
Krystyna Tatarkiewicz ◽  
Emmanuel J. Sablan ◽  
Clara J. Polizzi ◽  
Christiane Villescaz ◽  
David G. Parkes
Keyword(s):  
Body Weight ◽  
Gastric Emptying ◽  
Food Intake ◽  
High Fat Diet ◽  
Tolerance Test ◽  
Metabolic Effects ◽  
Oral Glucose ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Glucagon-like peptide 1 receptors (GLP-1R) are expressed in multiple tissues and activation results in metabolic benefits including enhanced insulin secretion, slowed gastric emptying, suppressed food intake, and improved hepatic steatosis. Limited and inconclusive knowledge exists regarding whether the effects of chronic exposure to a GLP-1R agonist are solely mediated via this receptor. Therefore, we examined 3-mo dosing of exenatide in mice lacking a functional GLP-1R (Glp1r−/−). Exenatide (30 nmol·kg−1·day−1) was infused subcutaneously for 12 wk in Glp1r−/− and wild-type (Glp1r+/+) control mice fed a high-fat diet. Glycated hemoglobin A1c (HbA1c), plasma glucose, insulin, amylase, lipase, alanine aminotransferase (ALT), aspartate aminotransferase (AST), body weight, food intake, terminal hepatic lipid content (HLC), and plasma exenatide levels were measured. At the end of the study, oral glucose tolerance test (OGTT) and rate of gastric emptying were assessed. Exenatide produced no significant changes in Glp1r−/− mice at study end. In contrast, exenatide decreased body weight, food intake, and glucose in Glp1r+/+ mice. When compared with vehicle, exenatide reduced insulin, OGTT glucose AUC0–2h, ALT, and HLC in Glp1r+/+ mice. Exenatide had no effect on plasma amylase or lipase levels. Exenatide concentrations were approximately eightfold higher in Glp1r−/− versus Glp1r+/+ mice after 12 wk of infusion, whereas renal function was similar. These data support the concept that exenatide requires a functional GLP-1R to exert chronic metabolic effects in mice, and that novel “GLP-1” receptors may not substantially contribute to these changes. Differential exenatide plasma levels in Glp1r+/+ versus Glp1r−/− mice suggest that GLP-1R may play an important role in plasma clearance of exenatide and potentially other GLP-1-related peptides.

scholarly journals Dietary Supplementation of Strawberry Improves Vascular Inflammation Without Altering Metabolic Milieu in High-fat Diet Fed C57BL/6 J Mice (P06-086-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
James Miller ◽  
Madison N Putich ◽  
Jennifer E Mueller ◽  
Aubrey O'Farrell ◽  
Samira Sholami ◽  
...  
Keyword(s):  
Body Weight ◽  
Blood Glucose ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Vascular Inflammation ◽  
Fasting Blood Glucose ◽  
Vascular Complications ◽  
High Fat ◽  
Dark Cycle ◽  
Insulin Tolerance

Abstract Objectives Metabolic syndrome (MetS) is an important risk factor for cardiovascular mortality and vascular inflammation plays a major role in the development of vascular complications. We tested the hypothesis that dietary strawberries (SB) attenuate vascular inflammation in MetS and this is due to a direct effect of SB on the vasculature. Methods Seven-week-old male C57BL/6 J mice consumed rodent diets with 10% kcal from fat (control diet fed mice; CD) or 60% kcal from fat (high-fat diet fed mice; HFD) for 12 weeks and subgroups of CD and HFD mice were fed a 2.35% freeze-dried SB supplemented diet (CD + SB or HFD + SB). This dose in mice is equivalent to two servings of SB (∼160 g) per day in humans. HFD model shares many vascular phenotypes with human MetS including vascular inflammation. The following analyses were completed after 12-week treatment: body weight; food intake; body composition; respiratory exchange ratio (RER), energy expenditure and activity (in light and dark cycle by Comprehensive Laboratory Animal Monitoring System); fasting and non-fasting blood glucose; glucose and insulin tolerance tests; and vascular inflammation (binding of fluorescent labelled mouse monocytes WEHI78/24 to aortic vessel). Results HFD mice exhibited increased body weight, reduced lean body mass, increased body fat, reduced RER (in both light and dark cycle), increased fasting and non-fasting blood glucose, and impaired glucose and insulin tolerance compared to CD mice (P < 0.05). SB supplementation does not alter body weight, body fat, lean body mass, blood glucose, glucose or insulin tolerance in CD + SB and HFD + SB mice. The energy expenditure and activity were similar among the groups. The aortic vessel from HFD exhibited an increased binding to WEHI 78/24 monocytic cells vs CD mice. However, SB supplementation reduced monocyte binding to the vessel in HFD + SB vs HFD mice (P < 0.05). Conclusions Strawberry supplementation improves vascular inflammation in HFD mice without altering metabolic milieu. This study indicates that the beneficial vascular effects of SB may not be due to a secondary effect but could be a direct effect on the vasculature. Strawberry consumption may be a potential adjunct strategy to prevent vascular complications in MetS. Funding Sources USDA grant (to ABPV), University of Utah Undergraduate Research Opportunity Program Award (to MNP, JEM, ASO, SS).

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