Kudzu (Pueraria lobata) Vine Isoflavone, Puerarin, Improves Weight gain, Glucose Metabolism and Osteoporosis and Their Biokinetics in Ovariectomized Mouse

2017 ◽  
Vol 7 (3) ◽  
Author(s):  
Yukio Kawamura
Keyword(s):  
Weight Gain ◽  
Glucose Metabolism ◽  
Pueraria Lobata ◽  
Ovariectomized Mouse

scholarly journals Effects of sleeve gastrectomy and ileal transposition, alone and in combination, on food intake, body weight, gut hormones, and glucose metabolism in rats

2013 ◽  
Vol 305 (4) ◽  
pp. E507-E518 ◽  
Author(s):  
S. Nausheen ◽  
I. H. Shah ◽  
A. Pezeshki ◽  
D. L. Sigalet ◽  
P. K. Chelikani
Keyword(s):  
Body Weight ◽  
Sleeve Gastrectomy ◽  
Weight Gain ◽  
Food Intake ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Gut Hormones ◽  
Ileal Transposition ◽  
Gastric Restriction ◽  
Peripheral Tissues

Bariatric surgeries are hypothesized to produce weight loss and improve diabetes control by multiple mechanisms including gastric restriction and lower gut stimulation; the relative importance of these mechanisms remains poorly understood. We compared the effects of a typical foregut procedure, sleeve gastrectomy, (SG) with a primarily hindgut surgery, ileal transposition (IT), alone and together (SGIT), or sham manipulations, on food intake, body weight, gut hormones, glucose tolerance, and key markers of glucose homeostasis in peripheral tissues of adult male Sprague-Dawley rats (450–550 g, n = 7–9/group). SG, IT, and SGIT surgeries produced transient reduction in food intake and weight gain; the effects of SG and IT on intake and body weight were nonadditive. SG, IT, and SGIT surgeries resulted in increased tissue expression and plasma concentrations of the lower gut hormones glucagon-like peptide-1 and peptide YY and decreased plasma glucose-dependent insulinotropic peptide, insulin, and leptin concentrations. Despite transient effects on intake and weight gain, the SG, IT, and SGIT surgeries produced a significant improvement in glucose tolerance. In support of glycemic improvements, the protein abundance of key markers of glucose metabolism (e.g., GLUT4, PKA, IRS-1) in muscle and adipose tissue were increased, whereas the expression of key gluconeogenic enzyme in liver (G-6-Pase) were decreased following the surgeries. Therefore, our data suggest that enhanced lower gut stimulation following SG, IT, and SGIT surgeries leads to transient reduction in food intake and weight gain together with enhanced secretion of lower gut hormones and improved glucose clearance by peripheral tissues.

scholarly journals Antipsychotics and glucose metabolism: how brain and body collide

2019 ◽  
Vol 316 (1) ◽  
pp. E1-E15 ◽  
Author(s):  
Chantel Kowalchuk ◽  
Laura N. Castellani ◽  
Araba Chintoh ◽  
Gary Remington ◽  
Adria Giacca ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Weight Gain ◽  
Glucose Metabolism ◽  
First Generation ◽  
Clinical Evidence ◽  
Mental Illnesses ◽  
Therapeutic Effects ◽  
Direct Effects ◽  
Increased Risk

Since the serendipitous discovery of the first antipsychotic (AP) drug in the 1950s, APs remain the cornerstone of treatment for schizophrenia. A shift over the past two decades away from first-generation, conventional APs to so-called “atypical” (or 2nd/3rd generation) APs parallels acknowledgment of serious metabolic side-effects associated in particular with these newer agents. As will be reviewed, AP drugs and type 2 diabetes are now inextricably linked, contributing to the three- to fivefold increased risk of type 2 diabetes observed in schizophrenia. However, this association is not straightforward. Biological and lifestyle-related illness factors contribute to the association between type 2 diabetes and metabolic disease independently of AP treatment. In addition, APs have a well-established weight gain propensity which could also account for elevated risk of insulin resistance and type 2 diabetes. However, compelling preclinical and clinical evidence now suggests that these drugs can rapidly and directly influence pathways of glucose metabolism independently of weight gain and even in absence of psychiatric illness. Mechanisms of these direct effects remain poorly elucidated but may involve central and peripheral antagonism of neurotransmitters implicated not only in the therapeutic effects of APs but also in glucose homeostasis, possibly via effects on the autonomic nervous system. The clinical relevance of studying “direct” effects of these drugs on glucose metabolism is underscored by the widespread use of these medications, both on and off label, for a growing number of mental illnesses, extending safety concerns well beyond schizophrenia.

scholarly journals Chronic dietary erythritol exposure elevates fasting plasma erythritol levels but does not cause weight gain or modify glucose homeostasis in mice

2021 ◽  
Author(s):  
Semira R. Ortiz ◽  
Martha S. Field
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Uncoupling Protein ◽  
Disease Onset ◽  
Cardiometabolic Disease ◽  
Brown Adipose ◽  
Ucp1 Expression ◽  
Old Mice

AbstractObjectiveErythritol is both a common non-nutritive sweetener (NNS) and an endogenous product of glucose metabolism. Recent reports indicate that elevated plasma erythritol is a predictive biomarker of cardiometabolic disease onset and complications. Although short-term erythritol consumption has been evaluated, the effect of chronically elevated circulating erythritol on adiposity and glucose metabolism has not. This study investigated the effect of longer-term erythritol consumption on weight gain and glucose tolerance, and the interaction between dietary composition and erythritol supplementation on these parameters.Methods8-week-old and 20-week-old C57BL/6J mice were randomized to consume low-fat diet (LFD), high-fat diet (HFD), LFD with 40g/kg erythritol (LFD+ERY), and HFD with 40g/kg erythritol (HFD+ERY) groups. After 8 weeks, plasma erythritol, body weight and composition, food intake, glucose tolerance, and brown adipose tissue (BAT) uncoupling protein 1 (UCP1) expression were measured.ResultsPlasma erythritol was elevated 40-fold in mice consuming LFD+ERY or HFD+ERY relative to mice consuming LFD or HFD, respectively. Liver and kidney tissue contained higher levels of erythritol than adipose. Unexpectedly, there was no effect of erythritol supplementation on body weight or glucose tolerance in 8- or 20-week-old mice fed LFD+ERY, or in 8-week-old mice fed HFD+ERY. In 20-week-old mice fed HFD+ERY, there was a significant interaction between erythritol and body weight (p<0.0001) compared to controls, but the main effect of diet was not significant. We also found no effect of chronic erythritol consumption on BAT UCP1 expression.ConclusionProlonged erythritol consumption did not significantly impact body weight, composition, or glucose tolerance. This suggests that dietary erythritol does not contribute to the development of cardiometabolic disease.

Improved glucose metabolism and decreased weight gain in leptin-resistant, IGFBP2-deficient, db/db mice induced by AZP-3404, a 9-amino acid analog of IGFBP2

2021 ◽  
Author(s):  
Michael D. Culler ◽  
Stéphane Milano ◽  
Michel Ovize ◽  
Thomas Delale ◽  
der Lelij Aart Jan van ◽  
...  
Keyword(s):  
Weight Gain ◽  
Amino Acid ◽  
Glucose Metabolism ◽  
Acid Analog ◽  
Amino Acid Analog

scholarly journals Anti-Obesity Effects of Tanshinone I from Salvia miltiorrhiza Bunge in Mice Fed a High-Fat Diet through Inhibition of Early Adipogenesis

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1242
Author(s):  
Dae Young Jung ◽  
Ji-Hyun Kim ◽  
Myeong Ho Jung
Keyword(s):  
Cell Cycle ◽  
Body Weight ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
Salvia Miltiorrhiza ◽  
Obese Mice ◽  
High Fat ◽  
Salvia Miltiorrhiza Bunge

Tanshinone I (Tan I) is a diterpenoid isolated from Salvia miltiorrhiza Bunge and exhibits antitumor effects in several cancers. However, the anti-obesity properties of Tan I remain unexplored. Here, we evaluated the anti-obesity effects of Tan I in high-fat-diet (HFD)-induced obese mice and investigated the underlying molecular mechanisms in 3T3-L1 cells. HFD-induced obese mice were orally administrated Tan I for eight weeks, and body weight, weight gain, hematoxylin and eosin staining and serum biological parameters were examined. The adipogenesis of 3T3-L1 preadipocytes was assessed using Oil Red O staining and measurement of intracellular triglyceride (TG) levels, and mitotic clonal expansion (MCE) and its related signal molecules were analyzed during early adipogenesis of 3T3-L1 cells. The administration of Tan I significantly reduced body weight, weight gain, and white adipocyte size, and improved obesity-induced serum levels of glucose, free fatty acid, total TG, and total cholesterol in vivo in HFD-induced obese mice. Furthermore, Tan I-administered mice demonstrated improvement of glucose metabolism and insulin sensitivity. Treatment with Tan I inhibited the adipogenesis of 3T3-L1 preadipocytes in vitro, with this inhibition mainly occurring at an early phase of adipogenesis through the attenuation of MCE via cell cycle arrest at the G1/S phase transition. Tan I inhibited the phosphorylation of p38, extracellular signal-regulated kinase (ERK), and Akt during the process of MCE, while it stimulated the phosphorylation of AMP-activated protein kinase. Furthermore, Tan I repressed the expression of CCAAT-enhancer-binding protein β (C/EBPβ), histone H3K9 demethylase JMJD2B, and subsequently cell cycle genes. Moreover, Tan I regulated the expression of early adipogenic transcription factors including GATAs and Kruppel-like factor family factors. These results indicate that Tan I prevents HFD-induced obesity via the inhibition of early adipogenesis, and thus improves glucose metabolism and insulin sensitivity. This suggests that Tan I possesses therapeutic potential for the treatment of obesity and obesity-related diseases.

Skeletal muscle glucose metabolism in obesity-prone and obesity-resistant rats

1993 ◽  
Vol 264 (6) ◽  
pp. R1224-R1228 ◽  
Author(s):  
M. J. Pagliassotti ◽  
K. A. Shahrokhi ◽  
J. O. Hill
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Weight Gain ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glycogen Synthase ◽  
Body Weight Gain ◽  
Glycogen Synthesis ◽  
Insulin Resistant ◽  
Wide Range

Ad libitum access to a high-fat (HF) diet produces a wide range of weight gain in rats. Rats most susceptible to weight gain on such a diet (obesity prone; OP) are more insulin resistant after 4-5 wk of diet exposure than are those most resistant (obesity resistant; OR) to weight gain. To investigate whether skeletal muscle glucose metabolism contributes to insulin resistance in this model, insulin-stimulated glucose metabolism was assessed in the perfused hindquarter of rats exposed to either a low-fat (LF, n = 6) or HF diet for 5 wk. Delineation of OP (n = 6) and OR (n = 6) rats was based on body weight gain. OP rats gained 60% more body weight while eating only 10% more energy than OR rats. Single-pass perfusions were carried out for 2 h in the presence of glucose, insulin, and [U-14C]glucose. Insulin-stimulated glucose uptake (mumol.100 g-1.min-1) was 14.2 +/- 0.9 in LF, 11.1 +/- 0.8 in OR, and 6.2 +/- 0.6 in OP. Glucose oxidation (mumol.100 g-1.min-1) was 1.7 +/- 0.3 and 1.2 +/- 0.3 in LF and OR, respectively, but was 0.2 +/- 0.1 in OP. Net glycogen synthesis was significantly reduced in OP compared with OR and LF despite similar glycogen synthase I activity. Muscle triglyceride concentration was not significantly different in OR and OP rats. These results demonstrate significant defects in skeletal muscle glucose uptake and disposal in rats most susceptible to HF diet-induced obesity. Clearly, the heterogeneous response to a HF diet involves not only body weight gain but also skeletal muscle fuel metabolism.

scholarly journals Single or combined ablation of peripheral serotonin and p21 limit adipose tissue expansion and metabolic alterations in early adulthood in mice fed a normocaloric diet

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0255687
Author(s):  
Enrica Saponara ◽  
Rong Chen ◽  
Theresia Reding ◽  
Richard Zuellig ◽  
Darren C. Henstridge ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Glucose Metabolism ◽  
Tryptophan Hydroxylase ◽  
Kinase Inhibitor ◽  
Early Adulthood ◽  
Tissue Expansion ◽  
Tissue Mass ◽  
Metabolic Alterations ◽  
Novel Treatments

Identifying the fundamental molecular factors that drive weight gain even in the absence of hypercaloric food intake, is crucial to enable development of novel treatments for the global pandemic of obesity. Here we investigated both adipose tissue-specific and systemic events that underlie the physiological weight gain occurring during early adulthood in mice fed a normocaloric diet. In addition, we used three different genetic models to identify molecular factors that promote physiological weight gain during normocaloric and hypercaloric diets. We demonstrated that normal physiological weight gain was accompanied by an increase in adipose tissue mass and the presence of cellular and metabolic signatures typically found during obesity, including adipocyte hypertrophy, macrophage recruitment into visceral fat and perturbed glucose metabolism. At the molecular level, this was associated with an increase in adipose tissue tryptophan hydroxylase 1 (Tph1) transcripts, the key enzyme responsible for the synthesis of peripheral serotonin. Genetic inactivation of Tph1 was sufficient to limit adipose tissue expansion and associated metabolic alterations. Mechanistically, we discovered that Tph1 inactivation resulted in down-regulation of cyclin-dependent kinase inhibitor p21Waf1/Cip1 expression. Single or double ablation of Tph1 and p21 were equally effective in preventing adipocyte expansion and systemic perturbation of glucose metabolism, upon both normocaloric and hypercaloric diets. Our results suggest that serotonin and p21 act as a central molecular determinant of weight gain and associated metabolic alterations, and highlights the potential of targeting these molecules as a pharmacologic approach to prevent the development of obesity.

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