Inhibition of gastric inhibitory polypeptide signaling prevents obesity
By K. Miyawaki, Yuichiro Yamada, N. Ban, Y. Ihara, K. Tsukiyama, Heying Zhou, S. Fujimoto, A. Oku, K. Tsuda, S. Toyokuni and 11 more. Nature Medicine, 2002
957 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Endocrine and Autonomic Systems, Endocrinology, Diabetes and Metabolism
View Paper: https://www.semanticscholar.org/paper/d63a8189964f7ff1758023bee042573a8fb85e23
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In Cellular and Molecular Neuroscience
In Endocrine and Autonomic Systems
In Endocrinology, Diabetes and Metabolism
Citations in the corpus
- LY3298176, a novel dual GIP and GLP-1 receptor agonist for the treatment of type 2 diabetes mellitus: From discovery to clinical proof of concept (2018, background): “Observations from genetically modified mice are confounding as both GIPR-deficient [27] and GIP-overexpressing mice [30] seem to be protected from obesity.”
- Incretin hormones: Their role in health and disease (2018, background): “A role for GIP as an obesigenic signal from the gut is mainly based on animal studies looking at the consequences of GIP receptor knockout: GIP receptor knock-out mice do not become obese when fed a high-fat diet.(48) This may be functionally related to increased hexose absorption from the gut(68) a”
- Pharmacology, physiology, and mechanisms of incretin hormone action. (2013, background): “…the rodent GIPR increases the uptake of lipids, enhances adipokine secretion, and promotes weight gain, expansion of adipose tissue depots, and insulin resistance (Figure 5) (Lamont and Drucker, 2008), whereas Gipr / mice are protected from high-fat-feedinginduced obesity (Miyawaki et al., 2002).”
- Gut hormones and the regulation of energy homeostasis (2006, background): “The reason for this resistance is unclear and there has been speculation that it might reflect a direct effect on adipocytes rather than on central appetite-regulating circuit”
- Unimolecular Dual Incretins Maximize Metabolic Benefits in Rodents, Monkeys, and Humans (2013, background): “Finally, preclinical observations with GIPR knockout rodents reported less weight gain on a high-fat diet challenge and an overall protection from glycemic disturbances (6, 7), which was also observed with pharmacological GIP antagonism (9–11) and with transgenic ablation of GIP-producing intestinal”
- Enhancing incretin action for the treatment of type 2 diabetes. (2003, background): “Both peptides are equipotent and exhibit identical plasma half-lives and biological activities acting through the same receptor (6,7); however, the majority ( 80%) of circulating active GLP-1 appears to be GLP-1(7-36)amide (8).”
- The Role of Incretins in Glucose Homeostasis and Diabetes Treatment (2008, background): “Moreover, GIPR( / ) mice with defective leptin [GIPR( / ), Lepob/Lepob] are protected from dietinduced obesity and its associated complications that occur with defective leptin signaling, including T2DM and fatty liver (Miyawaki et al., 2002).”