Angiotensin Receptor and Tumor Necrosis Factor-α Activation Contribute to Glucose Intolerance Independent of Systolic Blood Pressure in Obese Rats (original) (raw)

2018, American journal of physiology. Renal physiology

Pathological activation of the renin-angiotensin system and inflammation are associated with hypertension and the development of metabolic syndrome (MetS). The contributions of angiotensin receptor type 1 (AT1) activation, independent of blood pressure, and inflammation on glucose intolerance and renal damage are not well defined. Using a rat model of MetS, we hypothesized that the onset of glucose intolerance is primarily mediated by AT1 activation and inflammation independent of elevated systolic blood pressure (SBP). In order to address this hypothesis, we measured changes in SBP, adiposity, plasma glucose, triglycerides, and glucose tolerance in six groups of rats: (1) lean, strain-control Long Evans Tokushima Otsuka (LETO; n=5), (2) obese Otsuka Long-Evans Tokushima Fatty (OLETF; n=8), (3) OLETF + angiotensin receptor blocker (ARB; 10 mg olmesartan/kg; n=8), (4) OLETF + tumor necrosis factor-α (TNF-α) inhibitor (ETAN; 1.25mg etanercept/kg; n=6), (5) OLETF + angiotensin receptor...

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