scholarly journals Polychlorinated Biphenyl 153 in Lipid Medium Modulates Differentiation of Human Adipocytes

2017 ◽  
pp. 653-662 ◽  
Author(s):  
D. MULLEROVA ◽  
M. PESTA ◽  
J. DVORAKOVA ◽  
M. CEDIKOVA ◽  
V. KULDA ◽  
...  
Keyword(s):  
Polychlorinated Biphenyl ◽  
High Fat ◽  
Vehicle Modeling ◽  
Protein Levels ◽  
Whole Process ◽  
Diet Induced Obesity ◽  
Master Genes ◽  
Phosphorylated Akt ◽  
Gene Expression Analyses ◽  
Lipid Vehicle

Emerging evidence indicates that polychlorinated biphenyls (PCBs) are involved in the development of diabetes mellitus in the obese. The purpose of this study was to determine mechanisms by which PCB 153 (2,2′,4,4′,5,5′-hexachloro-biphenyl) could influence diet-induced obesity and insulin resistance during adipogenesis. Lineage of h-ADMSCs was differentiated either as control (differentiation medium only), or with lipid vehicle modeling high fat nutrition (NuTRIflex) or lipid free vehicle (dimethylsulfoxide) for 28 days with or without PCB 153 daily co-exposure (in three concentrations 0.1, 1, and 10 µM). Gene expression analyses were performed using RT-qPCR at days 4, 10, 21, 24, 28; protein levels Akt and phosphorylated Akt (Phospho-Akt) by Western blot at days 4, and 21. PCB 153 treatment of h-ADMSCs only in lipid vehicle was associated with down regulation of key master genes of adipogenesis: PPARγ, SREBP-1, PPARGC1B, and PLIN2 during the whole process of differentiation; and with increased Akt and decreased Phospho-Akt protein level at day 21. We have shown that PCB 153, in concentration 0.1 µM, has a potential in lipid rich environment to modulate differentiation of adipocytes. Because European and U.S. adults have been exposed to PCB 153, this particular nutrient-toxicant interaction potentially impacts human obesity and insulin sensitivity.

scholarly journals Freeze-dried jaboticaba peel powder improves insulin sensitivity in high-fat-fed mice

2013 ◽  
Vol 110 (3) ◽  
pp. 447-455 ◽  
Author(s):  
Nathalia R. V. Dragano ◽  
Anne y Castro Marques ◽  
Dennys E. C. Cintra ◽  
Carina Solon ◽  
Joseane Morari ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Receptor ◽  
Tolerance Test ◽  
Protective Role ◽  
High Fat ◽  
Protein Levels ◽  
Diet Induced Obesity ◽  
Forkhead Box ◽  
Insulin Tolerance ◽  
Freeze Dried

The peel of the native Brazilian fruit jaboticaba is rich in anthocyanins, which are known for their anti-obesity effects in animal models. The aim of the present study was to evaluate the effects of freeze-dried jaboticaba peel powder (FDJPP) on a number of metabolic parameters in a model of diet-induced obesity. Mice (n 8 per group) were initially fed on a high-fat diet (HFD, 35 % w/w) for 4 weeks and then switched to a HFD supplemented with FDJPP (1, 2 or 4 % w/w) for an additional 6 weeks. Energy intake, weight loss, glucose tolerance, insulin resistance and lipid profile were determined, and the results were evaluated using ANOVA and Tukey's tests. The FDJPP exerted no protective effect on HFD-induced weight gain, hyperleptinaemia and glucose intolerance. However, the supplementation was effective to reduce insulin resistance, as evidenced in the insulin tolerance test, and subsequently confirmed by improved signal transduction through the insulin receptor/insulin receptor substrate-1/Akt/forkhead box protein pathway and by the attenuation of HFD-induced inflammation in the liver, verified by lower expressions of IL-1β and IL-6 and decreased phosphorylated IκB-α protein levels in all jaboticaba-treated mice. These results suggest that FDJPP may exert a protective role against obesity-associated insulin resistance.

scholarly journals Diet-induced obesity leads to the development of leptin resistance in vagal afferent neurons

2011 ◽  
Vol 301 (1) ◽  
pp. E187-E195 ◽  
Author(s):  
Guillaume de Lartigue ◽  
Claire Barbier de la Serre ◽  
Elvis Espero ◽  
Jennifer Lee ◽  
Helen E. Raybould
Keyword(s):  
High Fat Diet ◽  
Leptin Resistance ◽  
Afferent Neurons ◽  
High Fat ◽  
Leptin Signaling ◽  
Protein Levels ◽  
Diet Induced Obesity ◽  
Nodose Ganglia ◽  
Vagal Afferent

Ingestion of high-fat, high-calorie diets is associated with hyperphagia, increased body fat, and obesity. The mechanisms responsible are currently unclear; however, altered leptin signaling may be an important factor. Vagal afferent neurons (VAN) integrate signals from the gut in response to ingestion of nutrients and express leptin receptors. Therefore, we tested the hypothesis that leptin resistance occurs in VAN in response to a high-fat diet. Sprague-Dawley rats, which exhibit a bimodal distribution of body weight gain, were used after ingestion of a high-fat diet for 8 wk. Body weight, food intake, and plasma leptin levels were measured. Leptin signaling was determined by immunohistochemical localization of phosphorylated STAT3 (pSTAT3) in cultured VAN and by quantifaction of pSTAT3 protein levels by Western blot analysis in nodose ganglia and arcuate nucleus in vivo. To determine the mechanism of leptin resistance in nodose ganglia, cultured VAN were stimulated with leptin alone or with lipopolysaccharide (LPS) and SOCS-3 expression measured. SOCS-3 protein levels in VAN were measured by Western blot following leptin administration in vivo. Leptin resulted in appearance of pSTAT3 in VAN of low-fat-fed rats and rats resistant to diet-induced obesity but not diet-induced obese (DIO) rats. However, leptin signaling was normal in arcuate neurons. SOCS-3 expression was increased in VAN of DIO rats. In cultured VAN, LPS increased SOCS-3 expression and inhibited leptin-induced pSTAT3 in vivo. We conclude that VAN of diet-induced obese rats become leptin resistant; LPS and SOCS-3 may play a role in the development of leptin resistance.

Lipoic acid increases heat shock protein expression and inhibits stress kinase activation to improve insulin signaling in skeletal muscle from high-fat-fed rats

2009 ◽  
Vol 106 (4) ◽  
pp. 1425-1434 ◽  
Author(s):  
Anisha A. Gupte ◽  
Gregory L. Bomhoff ◽  
Jill K. Morris ◽  
Brittany K. Gorres ◽  
Paige C. Geiger
Keyword(s):  
Heat Shock ◽  
Soleus Muscle ◽  
Lipoic Acid ◽  
Insulin Signaling ◽  
Chow Diet ◽  
High Fat ◽  
Protein Levels ◽  
Phosphorylated Akt ◽  
Stress Kinase

The antioxidant α-lipoic acid (LA) has been shown to improve insulin action in high-fat (HF)-fed animal models, yet little is known about its underlying mechanisms of action. We hypothesize that LA acts by inducing heat shock proteins (HSPs), which then inhibit stress kinases known to interfere with insulin signaling intermediates. Male Wistar rats were fed a HF diet (60% calories from fat) for 6 wk, while controls received a chow diet (10% calories from fat). One-half of the rats in each group received daily LA injections (30 mg/kg body wt). In rats fed a HF diet, LA increased expression of HSP72 and activation of HSP25 in soleus muscle, but it had no effect on HSPs in muscle from chow-fed rats. LA treatment reduced phosphorylation of c-Jun NH2-terminal kinase (JNK) and inhibitor of κB kinase-β (IKKβ) activity (IκBα protein levels) in rats fed a HF diet and effectively restored insulin responsiveness, as seen by insulin-stimulated phosphorylated Akt/Akt and 2-deoxyglucose uptake in soleus muscle. LA also induced activation of p38 MAPK and AMP-activated protein kinase, proteins previously implicated in insulin-independent glucose uptake. In addition, acute LA treatment induced HSPs in vitro in L6 muscle cells and prevented the activation of JNK and IKKβ with stimulants such as anisomycin and TNF-α, respectively. In conclusion, our results suggest chronic LA treatment results in stress kinase inhibition and improved insulin signaling through a HSP-mediated mechanism.

scholarly journals Differential regulation of pancreatic digestive enzymes during chronic high-fat diet-induced obesity in C57BL/6J mice

2014 ◽  
Vol 112 (2) ◽  
pp. 154-161 ◽  
Author(s):  
Ruth Z. Birk ◽  
Isabel Rubio-Aliaga ◽  
Mark V. Boekschoten ◽  
Hila Danino ◽  
Michael Müller ◽  
...  
Keyword(s):  
Pancreatic Lipase ◽  
Digestive Enzymes ◽  
Digestive Enzyme ◽  
Pancreatic Tissue ◽  
Diet Group ◽  
High Fat ◽  
Transcript Levels ◽  
Protein Levels ◽  
Diet Induced Obesity ◽  
Post Transcriptional Regulation

Exocrine pancreatic digestive enzymes are essential for the digestion of dietary components and are regulated by them. Chronic excess dietary high fat (HF) consumption is a contributing factor of diet-induced obesity (DIO) and associated chronic diseases and requires adaptation by the pancreas. The aim of the present study was to investigate the effects of chronic HF diet feeding on exocrine pancreatic digestive enzyme transcript levels in DIO C57BL/6J mice. C57BL/6J mice were fed diets containing either 10 or 45 % energy (E%) derived from fat for 12 weeks (n 10 mice per diet group). Pancreatic tissue and blood samples were collected at 0, 4 and 12 weeks. The expression of a panel of exocrine pancreatic digestive enzymes was analysed using quantitative RT-PCR and Western blot analysis. The HF (45 E%) diet-fed C57BL/6J mice developed obesity, hyperleptinaemia, hyperglycaemia and hyperinsulinaemia. The transcript levels of pancreatic lipase (PL), pancreatic lipase-related protein 2 (PLRP2) and pancreatic phospholipase A2 (PLA2) were initially elevated; however, they were down-regulated to basal control levels at week 12. The transcript levels of colipase were significantly affected by diet and time. The protein levels of PL and PLRP2 responded to HF diet feeding. The transcript levels of amylase and proteases were not significantly affected by diet and time. The transcript levels of specific lipases in hyperinsulinaemic, hyperleptinaemic and hyperglycaemic DIO C57BL/6J mice are down-regulated. However, these mice compensate for this by the post-transcriptional regulation of the levels of proteins that respond to dietary fat. This suggests a complex regulatory mechanism involved in the modulation of fat digestion.

Glucagon under high fat diet induced obesity

2007 ◽  
Vol 115 (S 1) ◽  
Author(s):  
LC Bollheimer ◽  
H Wobser ◽  
CE Wrede ◽  
A Schäffler ◽  
J Schölmerich ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity

Dissociation between high fat diet-induced obesity (DIO) and insulin resistance: lessons from AHNAK knockout mice

2013 ◽  
Author(s):  
Maya Ramdas ◽  
Chava Harel ◽  
Natalia Krits ◽  
Michal Armoni ◽  
Eddy Karnieli
Keyword(s):  
Insulin Resistance ◽  
Knockout Mice ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity

Differential effects of genetically inherited - and high fat diet induced - obesity on spermatogenesis in adult male rats

2018 ◽  
Author(s):  
Sharvari Deshpande ◽  
Harishankar Nemani ◽  
Suresh Pothani ◽  
Nafisa Balasinor
Keyword(s):  
Adult Male ◽  
High Fat Diet ◽  
Male Rats ◽  
High Fat ◽  
Differential Effects ◽  
Diet Induced Obesity

Enzymatically Modified Isoquercitrin Attenuates High-Fat Diet-Induced Obesity

2016 ◽  
Vol 45 (4) ◽  
pp. 474-483 ◽  
Author(s):  
Yeojin Min ◽  
Taesun Park
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity
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