Nateglinide Suppresses Postprandial Hypertriglyceridemia in Zucker Fatty Rats and Goto-Kakizaki Rats: Comparison with Voglibose and Glibenclamide.

Mine, Tomoyuki; Miura, Kyoko; Kitahara, Yoshiro; Okano, Akira; Kawamori, Ryuzo

doi:10.1248/bpb.25.1412

Cited by 17 publications

(12 citation statements)

References 23 publications

(27 reference statements)

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“…Nateglinide, on the other hand, has been shown to impact not only the clearance rate of TG-rich lipoprotein but also hepatic synthesis and secretion of TGs by reducing portal free fatty acid levels after a meal-induced increase in insulin secretion. 22,23 In the current study, the nateglinide-mediated improvement of postprandial TG at 30 min, in particular, was significantly correlated with a beneficial alteration in insulin response. When interpreting the results of the current study, it is necessary to consider the relatively small sample size that was used, as this feature of the study design restricted the statistical power of our analysis.…”

Section: Discussionsupporting

confidence: 51%

Differential Therapeutic Effects of Nateglinide and Acarbose on Fasting and Postprandial Lipid Profiles: A Randomized Trial

Zhou

Deng

et al. 2015

Diabetes Technology & Therapeutics

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Section: Discussionsupporting

confidence: 51%

Differential Therapeutic Effects of Nateglinide and Acarbose on Fasting and Postprandial Lipid Profiles: A Randomized Trial

Zhou

Deng

et al. 2015

Diabetes Technology & Therapeutics

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“…Individual compound doses were carefully selected according to standard dose ranges used in diabetic rat models, as reported previously for empagliflozin (Luippold et al, 2012;Thomas et al, 2012), liraglutide (Sturis et al, 2003;Brand et al, 2009;Schwasinger-Schmidt et al, 2013), and glibenclamide (Margolis 1987;Mine et al, 2002;Someya et al, 2009). Because rodents and humans display different pharmacokinetics, it should be noted that the dose ranges applied in preclinical diabetes studies are generally lower than that used in diabetic patients, that is, dosing regimens cannot directly be translated to clinical settings.…”

Section: Discussionmentioning

confidence: 99%

The Sodium Glucose Cotransporter Type 2 Inhibitor Empagliflozin Preserves β-Cell Mass and Restores Glucose Homeostasis in the Male Zucker Diabetic Fatty Rat

Hansen

Jelsing

Hansen

et al. 2014

J Pharmacol Exp Ther

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Type 2 diabetes is characterized by impaired b-cell function associated with progressive reduction of insulin secretion and b-cell mass. Evidently, there is an unmet need for treatments with greater sustainability in b-cell protection and antidiabetic efficacy. Through an insulin and b cell-independent mechanism, empagliflozin, a specific sodium glucose cotransporter type 2 (SGLT-2) inhibitor, may potentially provide longer efficacy. This study compared the antidiabetic durability of empagliflozin treatment (10 mg/kg p.o.) against glibenclamide (3 mg/kg p.o.) and liraglutide (0.2 mg/kg s.c.) on deficient glucose homeostasis and b-cell function in Zucker diabetic fatty (ZDF) rats. Empagliflozin and liraglutide led to marked improvements in fed glucose and hemoglobin A1c levels, as well as impeding a progressive decline in insulin levels. In contrast, glibenclamide was ineffective. Whereas the effects of liraglutide were less pronounced at week 8 of treatment compared with week 4, those of empagliflozin remained stable throughout the study period. Similarly, empagliflozin improved glucose tolerance and preserved insulin secretion after both 4 and 8 weeks of treatment. These effects were reflected by less reduction in b-cell mass with empagliflozin or liraglutide at week 4, whereas only empagliflozin showed b-cell sparing effects also at week 8. Although this study cannot be used to dissociate the absolute antidiabetic efficacy among the different mechanisms of drug action, the study demonstrates that empagliflozin exerts a more sustained improvement of glucose homeostasis and b-cell protection in the ZDF rat. In comparison with other type 2 diabetic treatments, SGLT-2 inhibitors may through insulin-independent pathways thus enhance durability of b-cell protection and antidiabetic efficacy.

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“…[35][36][37] Serum insulin level of 16-week-ZF rats (6.30 ng/ml) was significantly higher than both ZDF and ZL rats. [38][39][40] The abnormally lower serum insulin level in ZDF rats is closely related to H 2 S metabolism. Both expression of CSE and H 2 S production rate in pancreatic islets were significantly higher in ZDF than in ZL or ZF rats (Figure 1b and c).…”

Section: Discussionmentioning

confidence: 99%

Pancreatic islet overproduction of H2S and suppressed insulin release in Zucker diabetic rats

Yang

Jia

et al. 2009

Laboratory Investigation

196

156

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Hydrogen sulfide (H 2 S) has been traditionally known for its toxic effects on living organisms. The role of H 2 S in the homeostatic regulation of pancreatic insulin metabolism has been unclear. The present study is aimed at elucidating the effect of endogenously produced H 2 S on pancreatic insulin release and its role in diabetes development. Diabetes development in Zucker diabetic fatty (ZDF) rats was evaluated in comparison with Zucker fatty (ZF) and Zucker lean (ZL) rats. Pancreatic H 2 S production and insulin release were also assayed. It was found that H 2 S was generated in rat pancreas islets, catalyzed predominantly by cystathionine g-lyase (CSE). Pancreatic CSE expression and H 2 S production were greater in ZDF rats than in ZF or ZL rats. ZDF rats exhibited reduced serum insulin level, hyperglycemia, and insulin resistance. Inhibition of pancreatic H 2 S production in ZDF rats by intraperitoneal injection of DL-propargylglycine (PPG) for 4 weeks increased serum insulin level, lowered hyperglycemia, and reduced hemoglobin A1c level (Po0.05). Although in ZF rats it also reduced pancreatic H 2 S production and serum H 2 S level, PPG treatment did not alter serum insulin and glucose level. Finally, H 2 S significantly increased K ATP channel activity in freshly isolated rat pancreatic b-cells. It appears that insulin release is impaired in ZDF because of abnormally high pancreatic production of H 2 S. New therapeutic approach for diabetes management can be devised based on our observation by inhibiting endogenous H 2 S production from pancreas. KEYWORDS: diabetes; hydrogen sulfide; insulin release; K ATP channel; pancreas; type 2 diabetes mellitus Known as a swamp gas or 'rotten egg' gas, hydrogen sulfide (H 2 S) has yielded a public image of air pollutant for centuries. Physiological importance of H 2 S as a gasotransmitter has been realized for less than a decade. Endogenous production of H 2 S from L-cysteine is catalyzed by cystathionine b-synthase (CBS) and/or cystathionine g-lyase (CSE) with ammonium and pyruvate as co-products. 1 This process occurs in different organs and tissues, such as neuronal, vascular, and intestinal tissues. 2 Physiological concentrations of circulating H 2 S have been reported in the range of 45-300 mM. 1 At this physiological range, exogenous H 2 S has been shown to relax different vascular tissues, including isolated rat aortae and perfused mesenteric artery bed. 3-5 Altered cell proliferation or apoptosis induced by H 2 S has also been widely reported. [6][7][8][9][10] Endogenous production and physiological function of H 2 S in pancreas have been studied with identification of both CBS and CSE in rat pancreatic tissues or cloned rat pancreatic b-cell line. 11,12 In recent years, pathophysiological implications of the CSE/H 2 S system in diabetes have been reported. 12 CSE mRNA expression and H 2 S formation in rat pancreas was significantly increased after diabetes induction by streptozotocin injection. 12 CBS expression was reported in pancreatic acinar cells. 13 Y...

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Nateglinide Suppresses Postprandial Hypertriglyceridemia in Zucker Fatty Rats and Goto-Kakizaki Rats: Comparison with Voglibose and Glibenclamide.

Cited by 17 publications

References 23 publications

Differential Therapeutic Effects of Nateglinide and Acarbose on Fasting and Postprandial Lipid Profiles: A Randomized Trial

Differential Therapeutic Effects of Nateglinide and Acarbose on Fasting and Postprandial Lipid Profiles: A Randomized Trial

The Sodium Glucose Cotransporter Type 2 Inhibitor Empagliflozin Preserves β-Cell Mass and Restores Glucose Homeostasis in the Male Zucker Diabetic Fatty Rat

Pancreatic islet overproduction of H2S and suppressed insulin release in Zucker diabetic rats

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