Nicotinic Acid Inhibits Glucose-Stimulated Insulin Secretion Via the G Protein-Coupled Receptor PUMA-G in Murine Islet β Cells

Li, Hong Ming; Zhang, Mei; Xu, Shaofeng; Li, Di Zheng; Zhu, Lin; Peng, Si Wu; Chen, Guo Qiang; Martin, Pamela M.; Ganapathy, Vadivel; Wei, Chiju

doi:10.1097/mpa.0b013e31820b4b23

Cited by 22 publications

(14 citation statements)

References 39 publications

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“…One possible explanation for the virtual absence of an insulin rebound in this situation is that NiAc inhibits insulin secretion. Indeed, NiAc-induced blunting of glucose-stimulated insulin secretion has been demonstrated in vitro (36,37), albeit at considerably higher NiAc concentrations than those achieved in the present study. Thus, timing gradual NiAc withdrawal to the fed state should minimize FFA rebound.…”

Section: Damage Control By Minimizing Ffa Reboundcontrasting

confidence: 40%

“…Second, excessive exposures can invoke additional complicating mechanisms beyond FFA lowering. Examples include hepatic DGAT2 inhibition with an IC 50 of 100 µM (13,35), suppression of glucose-mediated insulin secretion via direct activation of GPR109A in the islet observed at 100 µM (36,37), downregulation of phophodiesterase-3B in adipose tissue reported at an 10-fold higher dose of NiAc than used in the current study (9) but not occurring at the present dose level (10), and Toll-like receptor-4 signaling inhibition (38) observed at 100 µM. the potential for FFA lowering might in theory be greater in the fasting state, it has been suggested that antilipolysis in this situation may invoke a more powerful counter-regulatory response to defend the supply of the predominant oxidative fuel (20,30).…”

Section: Discussionmentioning

confidence: 99%

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Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats[S]

Kroon

Baccega

Olsen

et al. 2017

Journal of Lipid Research

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Section: Damage Control By Minimizing Ffa Reboundcontrasting

confidence: 40%

Section: Discussionmentioning

confidence: 99%

Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats[S]

Kroon

Baccega

Olsen

et al. 2017

Journal of Lipid Research

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“…However, our data demonstrated that treatment with niacin led to a significant improvement in insulin resistance in HFD‐fed obese mice (HOMA‐IR). GPR109A has been shown to be functionally expressed in both human and murine islet β‐cells (72, 73). Chen et al .…”

Section: Discussionmentioning

confidence: 99%

Niacin fine‐tunes energy homeostasis through canonical GPR109A signaling

Cao

Lai

et al. 2018

FASEB j.

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The incidence of overweight and obesity has become a global public health problem, constituting a major risk factor for numerous comorbidities. Despite tremendous efforts, effective pharmacological agents for the treatment of obesity are still limited. Here, we showed that in contrast to lactate receptor GPR81, niacin receptor GPR109A‐deficient mice had progressive weight gain and hepatic fat accumulation. Using high‐fat diet–induced mouse model of obesity, we demonstrated that niacin treatment apparently protected against obesity without affecting food intake in wild‐type mice but not in GPR109A‐deficient mice. Further investigation showed that niacin treatment led to a remarkable inhibition of hepatic de novo lipogenesis. Additionally, we demonstrated that niacin treatment triggered brown adipose tissue and/or white adipose tissue thermogenic activity via activation of GPR109A. Moreover, we observed that mice exposed to niacin exhibited a dramatic decrease in intestinal absorption of sterols and fatty acids. Taken together, our findings demonstrate that acting on GPR109A, niacin shows the potential to maintain energy homeostasis through multipathways, representing a potential approach to the treatment of obesity, diabetes and cardiovascular disease.—Ye, L., Cao, Z., Lai, X., Wang, W., Guo, Z., Yan, L., Wang, Y., Shi, Y., Zhou, N. Niacin fine‐tunes energy homeostasis through canonical GPR109A signaling. FASEB J. 33, 4765–4779 (2019). http://www.fasebj.org

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“…Invokes apoptotic pathways in neutrophils and some cancer cells (e.g., breast and colon cancer). [ 12 , 46 , 71 – 73 ] …”

Section: Introductionmentioning

confidence: 99%

Expression of fatty acid sensing G-protein coupled receptors in peripartal Holstein cows

Agrawal

Alharthi

Vailati-Riboni

et al. 2017

J Animal Sci Biotechnol

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BackgroundG-protein coupled receptors (GPCR), also referred as Free Fatty Acid Receptors (FFAR), are widely studied within human medicine as drug targets for metabolic disorders. To combat metabolic disorders prevalent in dairy cows during the transition period, which co-occur with negative energy balance and changes to lipid and glucose metabolism, it may be helpful to identify locations and roles of FFAR and other members of the GPCR family in bovine tissues.ResultsQuantitative RT-PCR (qPCR) of subcutaneous adipose, liver, and PMNL samples during the transition period (-10, +7, and +20 or +30 d) were used for expression profiling of medium- (MCFA) and long-chain fatty acid (LCFA) receptors GPR120 and GPR40, MCFA receptor GPR84, and niacin receptor HCAR2/3. Adipose samples were obtained from cows with either high (HI; BCS ≥ 3.75) or low (LO; BCS ≤ 3.25) body condition score (BCS) to examine whether FFAR expression is correlated with this indicator of health and body reserves. Supplementation of rumen-protected methionine (MET), which may improve immune function and production postpartum, was also compared with unsupplemented control (CON) cows for liver and blood polymorphonuclear leukocytes (PMNL) samples. In adipose tissue, GPR84 and GPR120 were differentially expressed over time, while GPR40 was not expressed; in PMNL, GPR40 was differentially expressed over time and between MET vs. CON, GPR84 expression differed only between dietary groups, and GPR120 was not expressed; in liver, GPCR were either not expressed or barely detectable.ConclusionsThe data indicate that there is likely not a direct role in liver for the selected GPCR during the transition period, but they do play variable roles in adipose and PMN. In future, these receptors may prove useful targets and/or markers for peripartal metabolism and immunity.Electronic supplementary materialThe online version of this article (doi:10.1186/s40104-017-0150-z) contains supplementary material, which is available to authorized users.

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Nicotinic Acid Inhibits Glucose-Stimulated Insulin Secretion Via the G Protein-Coupled Receptor PUMA-G in Murine Islet β Cells

Abstract: The results indicated that PUMA-G stimulation by NA in islet β cells inhibited GSIS likely via activation of the Gi signaling pathway.

Cited by 22 publications

References 39 publications

Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats[S]

Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats[S]

Niacin fine‐tunes energy homeostasis through canonical GPR109A signaling

Expression of fatty acid sensing G-protein coupled receptors in peripartal Holstein cows

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