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Title:
Roux-en-Y Gastric Bypass Reduces Lipid Overaccumulation in Liver by Upregulating Hepatic Autophagy in Obese Diabetic Rats | Obesity Surgery
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Background The decrease in lipotoxicity is one of the crucial mechanisms by which Roux-en-Y gastric bypass (RYGB) improves insulin sensitivity. Little work, however, has been performed to elucidate the exact mechanism of RYGB reducing hepatic lipid overaccumulation in response to heavy lipid and glucose challenge. Here, we explored the effects of RYGB on hepatic autophagy in obese diabetic rats. Methods Sprague–Dawley rats were divided into five groups: diabetic RYGB, diabetic RYGB sham, diabetic food restriction (FR), diabetic rats, and non-diabetic controls (n = 12/group). At 4-week post-operation, genetic and protein expressions of autophagy markers including Atg7 and Beclin 1 and the conversion of LC3 were examined with quantitative RT-PCR and Western blotting. Plasma glucagon-like peptide-1 (GLP-1) and triglyceride and total cholesterol levels in liver tissue were tested. Results In both genetic and protein levels, we observed a significant upregulated autophagy in liver at 4 weeks after RYGB. Restored autophagy in liver played a key role in reducing the hepatic lipid burden in obese diabetic rats. The marked increase of autophagy in liver after RYGB correlated well with the plasma GLP-1 level. Conclusions Our data demonstrate that RYGB significantly upregulated hepatic autophagy. We suggest that the effects of RYGB on autophagy in liver may be due to the increased GLP-1 level after surgery. Moreover, the activated autophagy in liver might play a key role in reducing the hepatic lipid overaccumulation after RYGB.
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Keywords {🔍}
pubmed, article, google, scholar, cas, autophagy, hepatic, diabetes, gastric, bypass, rouxeny, central, rygb, rats, surgery, lipid, liver, diabetic, insulin, type, metab, obese, glucose, glp, obes, privacy, cookies, content, protein, nature, cell, china, data, publish, research, search, obesity, overaccumulation, wang, ping, sensitivity, role, access, rat, surg, resistance, analysis, information, log, journal,
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dpp-iv-resistant triple-acting agonist low-dose streptozotocin-treated rat month download article/chapter insulin-resistant zucker rat dietary-induced insulin resistance high-fat diet-fed high fat-fed c57bl/6 protein kinase c-delta long-term fructose feeding high-fat-fed mice free fatty acids full article pdf hepatic lipid overaccumulation privacy choices/manage cookies gastric bypass surgery increases intestinal gluconeogenesis increased glp-1 level hepatic insulin sensitivity hepatic lipid burden metabolic roux-en improves insulin sensitivity significant upregulated autophagy peripheral insulin sensitivity conditions privacy policy upregulating hepatic autophagy defective hepatic autophagy euglycemic insulin clamp plasma glp-1 level obese diabetic rats diabetic food restriction european economic area 4-week post-operation quantitative rt-pcr improving postprandial glycaemia related subjects health examination surveys arch biochem biophys contributing authors declare autophagy fights disease intestinal epithelial autophagy china medical university nat rev mol annu rev genet potent glucose-lowering total cholesterol levels short-term follow physiol endocrinol metab outstanding scientific fund ping han unfolded protein response
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headline:Roux-en-Y Gastric Bypass Reduces Lipid Overaccumulation in Liver by Upregulating Hepatic Autophagy in Obese Diabetic Rats
description:The decrease in lipotoxicity is one of the crucial mechanisms by which Roux-en-Y gastric bypass (RYGB) improves insulin sensitivity. Little work, however, has been performed to elucidate the exact mechanism of RYGB reducing hepatic lipid overaccumulation in response to heavy lipid and glucose challenge. Here, we explored the effects of RYGB on hepatic autophagy in obese diabetic rats. Sprague–Dawley rats were divided into five groups: diabetic RYGB, diabetic RYGB sham, diabetic food restriction (FR), diabetic rats, and non-diabetic controls (n = 12/group). At 4-week post-operation, genetic and protein expressions of autophagy markers including Atg7 and Beclin 1 and the conversion of LC3 were examined with quantitative RT-PCR and Western blotting. Plasma glucagon-like peptide-1 (GLP-1) and triglyceride and total cholesterol levels in liver tissue were tested. In both genetic and protein levels, we observed a significant upregulated autophagy in liver at 4 weeks after RYGB. Restored autophagy in liver played a key role in reducing the hepatic lipid burden in obese diabetic rats. The marked increase of autophagy in liver after RYGB correlated well with the plasma GLP-1 level. Our data demonstrate that RYGB significantly upregulated hepatic autophagy. We suggest that the effects of RYGB on autophagy in liver may be due to the increased GLP-1 level after surgery. Moreover, the activated autophagy in liver might play a key role in reducing the hepatic lipid overaccumulation after RYGB.
datePublished:2014-07-04T00:00:00Z
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Autophagy
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Surgery
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description:The decrease in lipotoxicity is one of the crucial mechanisms by which Roux-en-Y gastric bypass (RYGB) improves insulin sensitivity. Little work, however, has been performed to elucidate the exact mechanism of RYGB reducing hepatic lipid overaccumulation in response to heavy lipid and glucose challenge. Here, we explored the effects of RYGB on hepatic autophagy in obese diabetic rats. Sprague–Dawley rats were divided into five groups: diabetic RYGB, diabetic RYGB sham, diabetic food restriction (FR), diabetic rats, and non-diabetic controls (n = 12/group). At 4-week post-operation, genetic and protein expressions of autophagy markers including Atg7 and Beclin 1 and the conversion of LC3 were examined with quantitative RT-PCR and Western blotting. Plasma glucagon-like peptide-1 (GLP-1) and triglyceride and total cholesterol levels in liver tissue were tested. In both genetic and protein levels, we observed a significant upregulated autophagy in liver at 4 weeks after RYGB. Restored autophagy in liver played a key role in reducing the hepatic lipid burden in obese diabetic rats. The marked increase of autophagy in liver after RYGB correlated well with the plasma GLP-1 level. Our data demonstrate that RYGB significantly upregulated hepatic autophagy. We suggest that the effects of RYGB on autophagy in liver may be due to the increased GLP-1 level after surgery. Moreover, the activated autophagy in liver might play a key role in reducing the hepatic lipid overaccumulation after RYGB.
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Roux-en-Y gastric bypass (RYGB)
Autophagy
Glucagon-like peptide-1 (GLP-1)
Surgery
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