scholarly journals Liraglutide protects pancreatic β-cells against free fatty acids in vitro and affects glucolipid metabolism in apolipoprotein E−/− mice by activating autophagy

2015 ◽  
Vol 12 (3) ◽  
pp. 4210-4218 ◽  
Author(s):  
JIA WANG ◽  
JIE WU ◽  
HONG WU ◽  
XINGZHEN LIU ◽  
YINGJIAN CHEN ◽  
...  
2010 ◽  
Vol 401 (4) ◽  
pp. 561-567 ◽  
Author(s):  
Koji Komiya ◽  
Toyoyoshi Uchida ◽  
Takashi Ueno ◽  
Masato Koike ◽  
Hiroko Abe ◽  
...  

Nature ◽  
2003 ◽  
Vol 422 (6928) ◽  
pp. 173-176 ◽  
Author(s):  
Yasuaki Itoh ◽  
Yuji Kawamata ◽  
Masataka Harada ◽  
Makoto Kobayashi ◽  
Ryo Fujii ◽  
...  

2008 ◽  
Vol 36 (5) ◽  
pp. 905-908 ◽  
Author(s):  
Noel G. Morgan ◽  
Shalinee Dhayal ◽  
Eleftheria Diakogiannaki ◽  
Hannah J. Welters

Chronic exposure of pancreatic β-cells to long-chain fatty acids can cause loss of secretory function and enhanced apoptosis by a process of ‘lipotoxicity’, which may be a contributory factor to the rising incidence of Type 2 diabetes in humans. However, when incubated in vitro, β-cells respond differentially to long-chain saturated and mono-unsaturated fatty acids, suggesting that these molecules may regulate cell functionality by different mechanisms. In particular, it is clear that, whereas saturated fatty acids [e.g. palmitate (C16:0)] exert detrimental effects on β-cells, the equivalent mono-unsaturated species [e.g. palmitoleate (C16:1)] are well tolerated. Indeed, mono-unsaturated species are potently cytoprotective. The present review explores the differential effects of these various fatty acids on β-cell viability and considers the possible mechanisms involved in cytoprotection by mono-unsaturates.


2003 ◽  
Vol 278 (22) ◽  
pp. 19709-19715 ◽  
Author(s):  
Vasilij Koshkin ◽  
Xiaolin Wang ◽  
Philipp E. Scherer ◽  
Catherine B. Chan ◽  
Michael B. Wheeler

Biology ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 128
Author(s):  
Yaser Albadr ◽  
Andrew Crowe ◽  
Rima Caccetta

The prevalence of type 2 diabetes mellitus is rising globally and this disease is proposed to be the next pandemic after COVID-19. Although the cause of type 2 diabetes mellitus is unknown, it is believed to involve a complex array of genetic defects that affect metabolic pathways which eventually lead to hyperglycaemia. This hyperglycaemia arises from an inability of the insulin-sensitive cells to sufficiently respond to the secreted insulin, which eventually results in the inadequate secretion of insulin from pancreatic β-cells. Several treatments, utilising a variety of mechanisms, are available for type 2 diabetes mellitus. However, more medications are needed to assist with the optimal management of the different stages of the disease in patients of varying ages with the diverse combinations of other medications co-administered. Throughout modern history, some lead constituents from ancient medicinal plants have been investigated extensively and helped in developing synthetic antidiabetic drugs, such as metformin. Teucrium polium L. (Tp) is a herb that has a folk reputation for its antidiabetic potential. Previous studies indicate that Tp extracts significantly decrease blood glucose levels r and induce insulin secretion from pancreatic β-cells in vitro. Nonetheless, the constituent/s responsible for this action have not yet been elucidated. The effects appear to be, at least in part, attributable to the presence of selected flavonoids (apigenin, quercetin, and rutin). This review aims to examine the reported glucose-lowering effect of the herb, with a keen focus on insulin secretion, specifically related to type 2 diabetes mellitus. An analysis of the contribution of the key constituent flavonoids of Tp extracts will also be discussed.


2006 ◽  
Vol 291 (5) ◽  
pp. E885-E890 ◽  
Author(s):  
Dominik G. Haider ◽  
Friedrich Mittermayer ◽  
Georg Schaller ◽  
Michaela Artwohl ◽  
Sabina M. Baumgartner-Parzer ◽  
...  

The detrimental effect of elevated free fatty acids (FFAs) on insulin sensitivity can be improved by thiazolidinediones (TZDs) in patients with type 2 diabetes mellitus. It is unknown whether this salutary action of TZD is associated with altered release of the insulin-mimetic adipocytokine visfatin. In this study, we investigated whether visfatin concentrations are altered by FFA and TZD treatment. In a randomized, double-blind, placebo-controlled, parallel-group study 16 healthy volunteers received an infusion of triglycerides/heparin to increase plasma FFA after 3 wk of treatment with rosiglitazone (8 mg/day, n = 8) or placebo ( n = 8), and circulating plasma visfatin was measured. As a corollary, human adipocytes were incubated with synthetic fatty acids and rosiglitazone to assess visfatin release in vitro. The results were that rosiglitazone treatment increased systemic plasma visfatin concentrations from 0.6 ± 0.1 to 1.7 ± 0.2 ng/ml ( P < 0.01). Lipid infusion caused a marked elevation of plasma FFA but had no effect on circulating visfatin in controls. In contrast, elevated visfatin concentrations in subjects receiving rosiglitazone were normalized by lipid infusion. In isolated adipocytes, visfatin was released into supernatant medium by acute addition and long-term treatment of rosiglitazone. This secretion was blocked by synthetic fatty acids and by inhibition of phosphatidylinositol 3-kinase or Akt. In conclusion, release of the insulin-mimetic visfatin may represent a major mechanism of metabolic TZD action. The presence of FFA antagonizes this action, which may have implications for visfatin bioactivity.


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