Abstract
L-carnitine administration effects on AMPK, APPL1 and PPAR? genes expression in the liver and serum adiponectin levels and HOMA-IR in type 2 diabetes rat model induced by STZ and nicotinamide
Highlights
Diabetes is a public health problem and its global prevalence was nearly 422 mil lion adults [1]
Because its beneficial effects were previously reported in diabetic rats, we evaluated L-carnitine effects on the expression of AMPK and PPARγ genes which are involved in lipid metabolism regulation
We randomly selected 24 male Wistar rats (200 ± 10 g weight), after 7 days acclimatization the animals were ran domly divided into three groups (n = 8) as follow; group 1, healthy control which did not receive any treatment, group 2, diabetic control which received a single dose of STZ (45 mg/kg) and nicotinamide (200 mg/kg) by i.p injection to induce diabetes, group 3, diabetic rats plus L-carnitine which re ceived a single dose of STZ (45 mg/kg) and nicotina
Summary
Diabetes is a public health problem and its global prevalence was nearly 422 mil lion adults [1]. AMPK (AMP-activated protein kinase) is an enzyme that plays a pivotal role in energy homeostasis It is known as cellular energy sensor which promotes catabolic pathways such as fatty acid β-oxidation, on the other hand; it inhibits syn thetic pathways (Gluconeogenesis and Lipogenesis) to increase cellenergy levels [4, 10]. There is strong evidence from hu man and animal studies that have shown that lipid accumulation leads to insulin resistance and other metabolic complications. It reported that car nitine supplementation improves insulin-stimulated glucose uptake [9]. Previous studies have shown that PPARγ effects are exerted through adipo genesis and affecting glucose and lipid homeostasis, inflammation [14]
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