NDLI: Nicotinamide Mononucleotide Prevents Free Fatty Acid-Induced Reduction in Glucose Tolerance by Decreasing Insulin Clearance

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Nicotinamide Mononucleotide Prevents Free Fatty Acid-Induced Reduction in Glucose Tolerance by Decreasing Insulin Clearance

Content Provider	MDPI
Author	Nahle, Ashraf Joseph, Yemisi Deborah Pereira, Sandra Mori, Yusaku Poon, Frankie Ghadieh, Hilda E. Ivovic, Aleksandar Desai, Tejas Ghanem, Simona S. Asalla, Suman Muturi, Harrison T. Jentz, Emelien M. Joseph, Jamie W. Najjar, Sonia M. Giacca, Adria
Copyright Year	2021
Description	The NAD-dependent deacetylase SIRT1 improves β cell function. Accordingly, nicotinamide mononucleotide (NMN), the product of the rate-limiting step in NAD synthesis, prevents β cell dysfunction and glucose intolerance in mice fed a high-fat diet. The current study was performed to assess the effects of NMN on β cell dysfunction and glucose intolerance that are caused specifically by increased circulating free fatty acids (FFAs). NMN was intravenously infused, with or without oleate, in C57BL/6J mice over a 48-h-period to elevate intracellular NAD levels and consequently increase SIRT1 activity. Administration of NMN in the context of elevated plasma FFA levels considerably improved glucose tolerance. This was due not only to partial protection from FFA-induced β cell dysfunction but also, unexpectedly, to a significant decrease in insulin clearance. However, in conditions of normal FFA levels, NMN impaired glucose tolerance due to decreased β cell function. The presence of this dual action of NMN suggests caution in its proposed therapeutic use in humans.
Starting Page	13224
e-ISSN	14220067
DOI	10.3390/ijms222413224
Journal	International Journal of Molecular Sciences
Issue Number	24
Volume Number	22
Language	English
Publisher	MDPI
Publisher Date	2021-12-08
Access Restriction	Open
Subject Keyword	International Journal of Molecular Sciences Endocrinology and Metabolism Type 2 Diabetes Insulin Resistance Insulin Clearance Sirts Glucose Tolerance Free Fatty Acids
Content Type	Text
Resource Type	Article

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