pyrophosphate has been researched along with Obesity* in 3 studies
3 other study(ies) available for pyrophosphate and Obesity
| Article | Year |
|---|---|
The IP6K Inhibitor LI-2242 Ameliorates Diet-Induced Obesity, Hyperglycemia, and Hepatic Steatosis in Mice by Improving Cell Metabolism and Insulin Signaling.
Topics: Animals; Diet; Diphosphates; Hyperglycemia; Inositol; Insulin; Insulin Resistance; Lipid Metabolism; Lipids; Liver; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease; Obesity | 2023 |
Development of Novel IP6K Inhibitors for the Treatment of Obesity and Obesity-Induced Metabolic Dysfunctions.
Obesity and obesity-induced metabolic dysfunctions are significant risk factors for nonalcoholic fatty liver disease and cardiovascular diseases. Thus, obesity is an economic and social burden in developed countries. Blocking the synthesis of inositol pyrophosphates by inositol hexakisphosphate kinase (IP6K) has been identified as a potential therapeutic strategy for obesity and related diseases. We have developed a novel and potent IP6K inhibitor Topics: Animals; Diphosphates; HCT116 Cells; Humans; Inositol Phosphates; Mice; Obesity; Phosphotransferases (Phosphate Group Acceptor) | 2022 |
Inositol pyrophosphates inhibit Akt signaling, thereby regulating insulin sensitivity and weight gain.
The inositol pyrophosphate IP7 (5-diphosphoinositolpentakisphosphate), formed by a family of three inositol hexakisphosphate kinases (IP6Ks), modulates diverse cellular activities. We now report that IP7 is a physiologic inhibitor of Akt, a serine/threonine kinase that regulates glucose homeostasis and protein translation, respectively, via the GSK3β and mTOR pathways. Thus, Akt and mTOR signaling are dramatically augmented and GSK3β signaling reduced in skeletal muscle, white adipose tissue, and liver of mice with targeted deletion of IP6K1. IP7 affects this pathway by potently inhibiting the PDK1 phosphorylation of Akt, preventing its activation and thereby affecting insulin signaling. IP6K1 knockout mice manifest insulin sensitivity and are resistant to obesity elicited by high-fat diet or aging. Inhibition of IP6K1 may afford a therapeutic approach to obesity and diabetes. Topics: Adipogenesis; Aging; Animals; Cell Culture Techniques; Diet; Diphosphates; Inositol; Inositol Phosphates; Insulin; Insulin Resistance; Mice; Obesity; Phosphorylation; Phosphotransferases (Phosphate Group Acceptor); Proto-Oncogene Proteins c-akt; Weight Gain | 2010 |