scholarly journals Targeting hepatic glucose metabolism in the treatment of type 2 diabetes

2016 ◽  
Vol 15 (11) ◽  
pp. 786-804 ◽  
Author(s):  
Amy K. Rines ◽  
Kfir Sharabi ◽  
Clint D. J. Tavares ◽  
Pere Puigserver
1998 ◽  
Vol 102 (3) ◽  
pp. 619-624 ◽  
Author(s):  
C Meyer ◽  
M Stumvoll ◽  
V Nadkarni ◽  
J Dostou ◽  
A Mitrakou ◽  
...  

2021 ◽  
Vol 18 (5) ◽  
pp. 995-999
Author(s):  
Yufang Liu ◽  
Fang Wang ◽  
Xiue Xu ◽  
Hui Cong ◽  
Guiyan Chen

Purpose: To study the effects of angiotensin-(1-7) (angiot (1-7) intervention on angiotensin converting enzyme (ACE)-angiot-(1-7)-Mas pathway, hepatic glucose metabolism, and insulin resistance in rats with type 2 diabetes. Methods: Thirty-six Sprague Dawley rats were randomly divided into normal control, diabetic control and study groups (12 rats per group). Rats in the normal group were fed normal feed, while rats in the observation and diabetic control groups were type-2 diabetes model, and were given subcutaneous injection of angiot-(1-7) for 8 weeks. Serum insulin resistance index (IRI) and fasting insulin (FINS) were assayed. Other parameters measured were the levels of ACE2 and Mas receptor mRNA in liver tissues. Results: The levels of FINS in the study and control groups decreased, relative to normal control, while the levels of IRI was elevated (p < 0.05). There were significant increases in study group levels of Mas and ACE2, while angiot-(1-7) was lower, relative to control group (p < 0.05). The expressions of ACE2 and Mas receptors in study and diabetic control rats groups were downregulated, when compared to normal control. The expressions of ACE2 and Mas receptors also decreased in the study group exposed to angiot-(1-7) (p < 0.05). Conclusion: Angiot-(1-7) significantly increases the levels of FINS and IR, improves hepatic glucose metabolism and enhances ACE2-angiot-(1-7)-Mas pathway. Thus, angiot-(1-7) may be a new drug candidate for the treatment of type 2 diabetes.


2004 ◽  
Vol 52 (6) ◽  
pp. 366-374 ◽  
Author(s):  
Ananda Basu ◽  
Pankaj Shah ◽  
Michael Nielsen ◽  
Rita Basu ◽  
Robert A. Rizza

2020 ◽  
Vol 318 (2) ◽  
pp. G370-G374 ◽  
Author(s):  
C. Robb Flynn ◽  
Vance L. Albaugh ◽  
Robyn A. Tamboli ◽  
Justin M. Gregory ◽  
Amma Bosompem ◽  
...  

Roux-en-Y gastric bypass surgery (RYGB) is known to improve whole-body glucose metabolism in patients with type 2 diabetes (T2D), although the mechanisms are not entirely clear and are likely multifactorial. The aim of this study was to assess fasting hepatic glucose metabolism and other markers of metabolic activity before and after RYGB in patients with and without T2D. Methods: Metabolic characteristics of patients who are obese with T2D were compared with those without the disease (non-T2D) before and 1 and 6 mo after RYGB. Fasting plasma insulin and the insulin:glucagon ratio were markedly reduced as early as 1 mo after RYGB in both patients with T2D and without T2D. Despite this reduction, endogenous glucose production and fasting plasma glucose levels were lower in both groups after RYGB, with the reductions being much larger in T2D. Plasma kisspeptin, an inhibitor of insulin secretion, was reduced only in T2D after surgery. Improved hepatic glucose metabolism and lower plasma kisspeptin in T2D after RYGB may link improved hepatic function with enhanced insulin responsiveness after surgery. NEW & NOTEWORTHY Our manuscript is the first, to the best of our knowledge, to present data showing that Roux-en-Y gastric bypass surgery (RYGB) lowers fasting kisspeptin levels in patients who are obese with type 2 diabetes. This lowering of kisspeptin is important because it could link improvements in liver glucose metabolism after RYGB with increased insulin responsiveness also seen after surgery.


2004 ◽  
Vol 52 (6) ◽  
pp. 366-374 ◽  
Author(s):  
Ananda Basu ◽  
Pankaj Shah ◽  
Michael Nielsen ◽  
Rita Basu ◽  
Robert A. Rizza

Glucose production is inappropriately increased in people with type 2 diabetes both before and after food ingestion. Excessive postprandial glucose production occurs in the presence of decreased and delayed insulin secretion and lack of suppression of glucagon release. These abnormalities in hormone secretion, coupled with impaired insulin-induced suppression of glucose production and stimulation of splanchnic glucose uptake, likely account in large part for the excessive amounts of glucose that reach the systemic circulation for disposal by peripheral tissues following food ingestion. In contrast, when adequate basal insulin concentrations are present, neither glucagon-induced stimulation of glucose production nor glucose-induced suppression of glucose production differs in diabetic and nondiabetic subjects matched for gender, age, and degree of obesity. However, when insulin secretion is defective, lack of suppression of glucagon can cause substantial hyperglycemia by enhancing rates of glucose production. Therefore, normalization of hepatic glucose metabolism in people with type 2 diabetes mellitus likely will require normalization of insulin and glucagon secretion as well as hepatic insulin action.


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