9-PAHSA and Insulin-Resistance

9-PAHSA has been researched along with Insulin-Resistance* in 2 studies

Other Studies

2 other study(ies) available for 9-PAHSA and Insulin-Resistance

ArticleYear
Palmitic Acid Hydroxystearic Acids Activate GPR40, Which Is Involved in Their Beneficial Effects on Glucose Homeostasis.
    Cell metabolism, 2018, 02-06, Volume: 27, Issue:2

    Palmitic acid hydroxystearic acids (PAHSAs) are endogenous lipids with anti-diabetic and anti-inflammatory effects. PAHSA levels are reduced in serum and adipose tissue of insulin-resistant people and high-fat diet (HFD)-fed mice. Here, we investigated whether chronic PAHSA treatment enhances insulin sensitivity and which receptors mediate PAHSA effects. Chronic PAHSA administration in chow- and HFD-fed mice raises serum and tissue PAHSA levels ∼1.4- to 3-fold. This improves insulin sensitivity and glucose tolerance without altering body weight. PAHSA administration in chow-fed, but not HFD-fed, mice augments insulin and glucagon-like peptide (GLP-1) secretion. PAHSAs are selective agonists for GPR40, increasing Ca

    Topics: Adiposity; Animals; Eating; Glucose; HEK293 Cells; Homeostasis; Humans; Inflammation; Insulin Resistance; Mice, Inbred C57BL; Palmitic Acid; Receptors, G-Protein-Coupled; Stearic Acids

2018
Acute and Repeated Treatment with 5-PAHSA or 9-PAHSA Isomers Does Not Improve Glucose Control in Mice.
    Cell metabolism, 2018, 08-07, Volume: 28, Issue:2

    Fatty acid esters of hydroxylated fatty acids (FAHFAs) were discovered as a novel class of endogenous mammalian lipids whose profound effects on metabolism have been shown. In the current study, in vitro and in vivo the metabolic effects of two of these FAHFAs, namely palmitic acid-5- (or -9) -hydroxy-stearic acid (5- or 9-PAHSA, respectively) were profiled. In DIO mice fed with differentially composed low- or high-fat diets, acute and subchronic treatment with 5-PAHSA and 9-PAHSA alone, or in combination, did not significantly improve the deranged metabolic status. Neither racemic 5- or 9-PAHSA, nor the enantiomers were able to: (1) increase basal or insulin-stimulated glucose uptake in vitro, (2) stimulate GLP-1 release from GLUTag cells, or (3) induce GSIS in rat, mouse, or human islets or in a human pancreatic β cell line. Therefore, our data do not support the further development of PAHSAs or their derivatives for the control of insulin resistance and hyperglycemia.

    Topics: Animals; Diet, Fat-Restricted; Diet, High-Fat; Glucagon-Like Peptide 1; Glucose; HEK293 Cells; Humans; Hyperglycemia; Insulin Resistance; Islets of Langerhans; Mice; Mice, Inbred C57BL; Models, Animal; Obesity; Palmitic Acid; Rats; Rats, Sprague-Dawley; Stearic Acids

2018