Published on : Sep 20, 2019
Albany, New York, September 20, 2019: Gastric inhibitory polypeptide receptor (GIPR) induces energy accumulation in adipose tissue in vitro. Nonetheless, gastric inhibitory polypeptide receptor becomes instrumental in lipid metabolism and is linked with insulin resistance and obesity. Several anti-obesity agents including sibutramine, orlistat and rimonabant have received green signal for clinical use in North America and Europe. GIP was initially identified as an activity in extracts which showed inhibited gastric acid secretion and gastrin release. Subsequently, gastric inhibitory polypeptide receptor exhibited to spur insulin release in the presence of increased glucose.
These insights are according to the intelligence report, titled, “Gastric Inhibitory Polypeptide Receptor—Pipeline Review, H2 2019,” which has been freshly added to Market Research Hub’s (MRH) overarching repository.
Gastric inhibitory polypeptide is an incretin secreted from enteroendocrine K cells in response to potentiates insulin secretin and meal ingestion through the gastric inhibitory polypeptide receptor. Several studies have revealed gastric inhibitory polypeptide induces energy accumulation in adipose tissue by augmenting lipoprotein lipase expression by propelling LPL enzyme activity.
Even though gastric inhibitory polypeptide function in human adipose tissue is obscure in vivo, in-vitro study infers that gastric inhibitory polypeptide (GIP) induces potentiates IL-6 secretion and IL-6 mRNA expression in the presence of TNF-alpha in human adipocytes. Nonetheless, gastric inhibitory polypeptide being witnessed in adipose tissue becomes significant in HFD-induced insulin resistance and hepatic steatosis in vivo.
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