Obese mice weight loss role on nonalcoholic fatty liver disease and endoplasmic reticulum stress treated by a GLP-1 receptor agonist.
Rayane Miranda Pontes-da-SilvaThatiany Souza MarinhoLuiz Eduardo Macedo CardosoCarlos Alberto Mandarim-de-LacerdaMarcia Barbosa AguilaPublished in: International journal of obesity (2005) (2021)
Semaglutide and the consequent weight loss reduced obese mice liver inflammation, insulin resistance, and ER stress. However, weight loss alone did show few or no action on some significant study findings, like liver steatosis, leptin, insulin, resistin, and amylin. Furthermore, hepatic inflammation mediated by MCP-1 and partially by TNF-alpha and IL6 were also not reduced by weight loss. Furthermore, weight loss alone did not lessen hepatic lipogenesis as determined by the findings of SREBP-1c, CHREBP, PPAR-alpha, and SIRT1. Semaglutide was implicated in improving glucose uptake and lessening ER stress by reducing GADD45, independent of weight loss.
Keyphrases
- weight loss
- bariatric surgery
- roux en y gastric bypass
- insulin resistance
- gastric bypass
- endoplasmic reticulum stress
- glycemic control
- oxidative stress
- type diabetes
- adipose tissue
- high fat diet
- weight gain
- induced apoptosis
- rheumatoid arthritis
- metabolic syndrome
- ischemia reperfusion injury
- blood pressure
- body mass index
- signaling pathway