Duodenal-Jejunal Bypass Surgery Ameliorates Glucose Homeostasis and Reduces Endoplasmic Reticulum Stress in the Liver Tissue in a Diabetic Rat Model

Li, Maogang; Li, Hengping; Zhou, Zhigang; Zhou, Yanggui; Wang, Yanmin; Zhang, Xiang; Li, Teng; Zhong, Maiying; Han, Huijian; Liu, Shaozhuang; Hu, Sanyuan

doi:10.1007/s11695-015-1816-2

Cited by 14 publications

(11 citation statements)

References 39 publications

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“…To establish the rat model of T2DM (Li et al, 2016; Ma et al, 2017), 60 male rats (80–100 g, 4-week old) were a fed high fat diet (HFD) (20% sugar, 10% lard, 10% egg yolk, and 60% basal feed) after a week of normal diet. After 4 weeks, rats were injected once with low-dose STZ (Solarbio, China) (STZ, 30 mg/kg i.p) to induce partial insulin deficiency, and then continuously fed HFD for 4 weeks after injection of STZ.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of COX2/PGD2-Related Autophagy Is Involved in the Mechanism of Brain Injury in T2DM Rat

Yang

Chen

Zhao

et al. 2019

Front. Cell. Neurosci.

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The present study was designed to observe the effect of COX2/PGD2-related autophagy on brain injury in type 2 diabetes rats. The histopathology was detected by haematoxylin–eosin staining. The learning and memory functions were evaluated by Morris water maze. The levels of insulin and PGD2 were measured by enzyme-linked immunosorbent assay. The expressions of COX2, p-AKT(S473), p-AMPK(T172), Aβ, Beclin1, LC3BII, and p62 were measured by immunohistochemistry and Western blotting. In model rats, we found that the body weight was significantly decreased, the blood glucose levels were significantly increased, the plasma insulin content was significantly decreased, the learning and memory functions were impaired and the cortex and hippocampus neurons showed significant nuclear pyknosis. The levels of COX2, p-AKT(S473), PGD2, Aβ, Beclin1 and p62 were significantly increased, whereas the expression of p-AMPK(T172) and LC3BII was significantly decreased in the cortex and hippocampus of model rats. In meloxicam-treated rats, the body weight, blood glucose and the content of plasma insulin did not significantly change, the learning and memory functions were improved and nuclear pyknosis was improved in the cortex and hippocampus neurons. The expression of p-AMPK(T172), Beclin1 and LC3BII was significantly increased, and the levels of COX2, p-AKT(S473), PGD2, Aβ, and p62 were significantly decreased in the cortex and hippocampus of meloxicam-treated rats. Our results suggested that the inhibition of COX2/PGD2-related autophagy was involved in the mechanism of brain injury caused by type 2 diabetes in rats.

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Section: Methodsmentioning

confidence: 99%

Inhibition of COX2/PGD2-Related Autophagy Is Involved in the Mechanism of Brain Injury in T2DM Rat

Yang

Chen

Zhao

et al. 2019

Front. Cell. Neurosci.

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“…To establish model of T2DM, male rats (80–100 g, 9-week-old) 49 were fed high fat diet (HFD) (20% sugar, 10% lard, 10% egg yolk and 60% basal feed) after a week of normal diet. After 4 weeks, rats were injected once with low-dose streptozotocin (Solarbio, China) (STZ, 30 mg/kg i.p) to induce partial insulin deficiency, and then continuously fed HFD for 4 weeks after injection of STZ.…”

Section: Methodsmentioning

confidence: 99%

CMD-05, a novel promising clinical anti-diabetic drug candidate, in vivo and vitro studies

et al. 2017

Sci Rep

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Dipeptidyl peptidase IV (DPP-IV) inhibitor has been expected to be a new class of anti-diabetic agent. The present study was designed to characterize the pharmacological profiles of CMD-05, a novel DPP-IV inhibitor discovered in our laboratory, in vitro and in vivo. The IC50 of CMD-05 on DPP-IV inhibitory activity was approximately 12 nM while vildagliptin was 3.5 nM in vitro. In diabetes rat model established by high fat diet/low dose streptozotocin, CMD-05 inhibited DPP-IV activity, significantly improved glucose tolerance, increased GLP-1 and insulin levels in plasma. Long-term administration of CMD-05 decreased HbA1c and TG levels and improved the islet function without significantly effect on body weight. Furthermore, CMD-05 reduced INS-1 cell apoptosis and increased GLP-1 secretion in NCI-H716. After oral administration, CMD-05 reached peak concentration at 30 min with half-life of 288 minutes and the inhibitory rate of DPP-IV greater than 50% lasted for 15 h. In fasted normal rats, CMD-05 didn’t cause significant hypoglycemia. CMD-05 had a lower cytotoxicity than vildagliptin in vitro and its maximum tolerance dose in mice is beyond 2000 mg/kg. These results indicated that CMD-05 has similar activity with vildagliptin in vivo and has a much longer half-life and lower cytotoxicity than vildagliptin.

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“…In addition to medication such as insulin and antidiabetic drugs, surgery is an important treatment strategy for diabetes. For example, duodenal-jejunal bypass (DJB) has been shown to be an effective surgical treatment for T2DM [141]. Meanwhile, miR-320 might mediate the therapeutic effects of DJB in T2DM.…”

Section: The Effects Of Mir-320 On Glucose and Lipid Metabolism In Thmentioning

confidence: 99%

The role of miR-320 in glucose and lipid metabolism disorder-associated diseases

Zhang

Yin

et al. 2021

Int. J. Biol. Sci.

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Duodenal-Jejunal Bypass Surgery Ameliorates Glucose Homeostasis and Reduces Endoplasmic Reticulum Stress in the Liver Tissue in a Diabetic Rat Model

Abstract: DJB ameliorates glucose homeostasis. Meanwhile, our study helps to reveal that the reduced hepatic ER stress and the decreased JNK activity may contribute to the improved glucose homeostasis after DJB.

Cited by 14 publications

References 39 publications

Inhibition of COX2/PGD2-Related Autophagy Is Involved in the Mechanism of Brain Injury in T2DM Rat

Inhibition of COX2/PGD2-Related Autophagy Is Involved in the Mechanism of Brain Injury in T2DM Rat

CMD-05, a novel promising clinical anti-diabetic drug candidate, in vivo and vitro studies

The role of miR-320 in glucose and lipid metabolism disorder-associated diseases

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