Duodenal–Jejunal Bypass Surgery Up-Regulates the Expression of the Hepatic Insulin Signaling Proteins and the Key Regulatory Enzymes of Intestinal Gluconeogenesis in Diabetic Goto–Kakizaki Rats

Sun, Dong; Wang, Kexin; Yan, Zhibo; Liu, Shaozhuang; Liu, Fengjun; Hu, Chun-Xiao; Hu, Sanyuan

doi:10.1007/s11695-013-0985-0

Cited by 35 publications

(29 citation statements)

References 40 publications

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“…It is strongly suggested that, intestinal glucose release may take place during the postabsorptive period after gastric bypass surgery in obese humans [49,50]. It must also be noted that data from our study in mice [48] have recently been supported by a similar study of bypass surgery in the Goto-Kakisaki diabetic rat [51]. Finally, it must be emphasized that intestinal gluconeogenesis curbing hunger sensation and improving insulin sensitivity, and glucagon-like peptide 1 secretion improving insulin secretion, may act in synergy to promote the whole beneficial effect of gastric bypass surgeries on glucose and energy homeostasis [52].…”

Section: Intestinal Gluconeogenesis In Gastric Bypasssupporting

confidence: 60%

Nutrient Control of Energy Homeostasis via Gut-Brain Neural Circuits

Mithieux

2014

Neuroendocrinology

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Intestinal gluconeogenesis is a recently described function in intestinal glucose metabolism. In particular, the intestine contributes around 20-25% of total endogenous glucose production during fasting. Intestinal gluconeogenesis appears to regulate energy homeostasis via a neurally mediated mechanism linking the enterohepatic portal system with the brain. The periportal neural system is able to sense glucose produced by intestinal gluconeogenesis in the portal vein walls, which sends a signal to the brain to modulate energy and glucose homeostasis. Dietary proteins mobilize intestinal gluconeogenesis as a mandatory link between the sensing of these proteins in the portal vein and their well-known effect of satiety. Comparably, dietary soluble fibers exert their antiobesity and antidiabetic effects via the induction of intestinal gluconeogenesis. Finally, intestinal gluconeogenesis might be involved in the rapid metabolic improvements in energy homeostasis induced by gastric bypass surgeries of obesity.

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Section: Intestinal Gluconeogenesis In Gastric Bypasssupporting

confidence: 60%

Nutrient Control of Energy Homeostasis via Gut-Brain Neural Circuits

Mithieux

2014

Neuroendocrinology

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“…Also, acute inhibition of glucose-6-phosphate translocator activity leads to increased de novo lipogenesis and development of hepatic steatosis without affecting VLDL production in rats [18]. It is worth mentioning that 20 weeks after duodenal -jejunal bypass in Goto-Kakizaki rats, G6PC levels within the liver were lower than in the SHAM operated group [9]. DJB operation consists of elements other than IT, but the effect could be similar, meaning low levels of G6PC in the liver.…”

Section: Discussionmentioning

confidence: 94%

“…All surgical and experimental procedures were precisely described earlier by our research group [3,13], thus in this paper we briefly present only the main points. The animal experimental protocols were approved by the Ethics Committee of the University of Freiburg [3,9,13]. In short, 11 to 12-week-old, 200-220 g, obese male Zucker rats (Crl:ZUC-Lepr fa ) were purchased from Charles River Breeding Laboratories (Wilmington, Mass).…”

Section: Methodsmentioning

confidence: 99%

“…It has been recognized that glucose-6-phosphatase (G6PC) is one of the crucial regulatory enzymes of gluconeogenesis and is expressed in the liver, skeletal muscle and small intestine [10]. Glycogen phosphorylase (PYGM) is the major enzyme in glycogenolysis responsible for the glucose-1-phosphate release from glycogen [9]. Glycogen synthase kinase-3 (GSK-3 EC 2.7.11.26) is involved in glycogen synthase (GS) regulation, phosphorylation and its deactivation.…”

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confidence: 99%

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Ileal transposition in rats influenced glucose metabolism and HSP70 levels

et al. 2015

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Objective: Ileal transposition procedure (IT), in combination with sleeve gastrectomy, is widely used to induce diabetes remission and to control related metabolic abnormalities. A transposition of a long segment of distal ileum in obese Zucker rats improved glucose tolerance 6 months after IT. The premise of our study was to to examine the long - term effects of ileum transposition on the liver glycolytic enzymes content in a euglycemic group of operated Zucker rats. Methods: Twenty male Zucker rats underwent either the transposition of 50% distal ileum or a sham surgery. Six months after surgery, liver tissue concentrations of glycogen synthase kinase alpha (GSK-3α), glucose 6-phosphatase (G6PC), glycogen phosphorylase (PYGM) and phosphofructokinase (PFK) and HSP70 were assessed by immunoenzymatic methods. Results: HSP70 values were significantly higher in the IT group compared to SHAM. G6PC liver concentrations in the IT group were almost 1.45-fold lower than in the SHAM operated rats. Statistical analyses (F-test) showed HSP70 levels were significantly related to caveolin-1and SHAM group. Conclusions: Lowered glycolytic enzyme concentrations assessed in the liver suggest positive effects on glucose metabolism in long-term observations.

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“…Simultaneously, PI3K-AKT activation phosphorylates Foxo1 proteins and decreases the expression of gluconeogenic genes, such as Pepck and G6pase [16]. Sun et al [34] found that duodenal-jejunal bypass could significantly downregulate the expression of the key regulatory enzymes of hepatic gluconeogenesis without weight loss in diabetic GK rats. However, Gerhard et al [35] reported that hepatic GS gene expression and glycogen content were not different between nondiabetic and diabetic patients, and no remission were observed in patients with diabetes after RYGB.…”

Section: Discussionmentioning

confidence: 99%

Roux-en-Y Gastric Bypass Improves Hepatic Glucose Metabolism Involving Down-Regulation of Protein Tyrosine Phosphatase 1B in Obese Rats

et al. 2017

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Objective: This study was initiated to investigate the effects of Roux-en-Y gastric bypass (RYGB) surgery on hepatic glucose metabolism and hepatic expression of protein tyrosine phosphatase 1B (PTP1B) in obese rats. Methods: Body weight, glucose, intraperitoneal glucose, insulin, and pyruvate tolerance tests were performed pre- and postoperatively, and plasma lipid, insulin and glucagon-like peptide 1 (GLP-1) were measured. The mRNA levels of G6Pase, Pepck, Gsk-3β and Gys-2, and the expression levels of PTP1B mRNA, protein, and other components of the insulin signaling pathway were measured by using RT-PCR and western blotting. The intracellular localization of PTP1B and hepatic glycogen deposition was also observed. Results: RYGB surgery-treated rats showed persistent weight loss, significantly improved glucose tolerance, pyruvate tolerance, and dyslipidemia, as well as increased insulin sensitivity, hepatic glycogen deposition and increased plasma GLP-1 in obese rats. RT-PCR analyses showed Pepck, G6Pase, and Gsk-3β mRNA to be significantly decreased, and Gys-2 mRNA to be significantly increased in liver tissue in the RYGB group (p < 0.05 vs. high-fat diet (HFD) or HFD + sham group); in addition, the expression of PTP1B were significantly decreased and insulin signaling were improved in the RYGB group (p < 0.05 vs. HFD or HFD + sham group). Conclusion: RYGB can improve hepatic glucose metabolism and down-regulate PTP1B in obese rats. An increased circulating GLP-1 concentration may be correlated with the effects following RYGB in obese rats.

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Duodenal–Jejunal Bypass Surgery Up-Regulates the Expression of the Hepatic Insulin Signaling Proteins and the Key Regulatory Enzymes of Intestinal Gluconeogenesis in Diabetic Goto–Kakizaki Rats

Cited by 35 publications

References 40 publications

Nutrient Control of Energy Homeostasis via Gut-Brain Neural Circuits

Nutrient Control of Energy Homeostasis via Gut-Brain Neural Circuits

Ileal transposition in rats influenced glucose metabolism and HSP70 levels

Roux-en-Y Gastric Bypass Improves Hepatic Glucose Metabolism Involving Down-Regulation of Protein Tyrosine Phosphatase 1B in Obese Rats

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