Abstract
Obesity is a notable risk factor for developing type 2 diabetes, augmenting the concern of obese diabetes (ObD). Anti-obesity and antioxidant effects of red pepper seeds extract (RPSE) have increased our expectations that RPSE would also improve the pathological phenotypes of obese diabetes. Therefore, we hypothesized that RPSE would have an anti-diabetic effect in ObD mice. Animals were assigned either as follows: (1) db/+, (2) db/db control, (3) RPSE (200 mg/kg bw), or (4) a comparative control (metformin 150 mg/kg bw). RPSE was orally administered daily for 8 weeks. As a result, RPSE supplementation improved diabetic phenotypes, including fasting glucose, hemoglobin (HbA1c), and insulin levels. Pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6), and triglycerides were reduced in RPSE-treated mice. RPSE supplementation also diminished the rate-limiting enzymes of gluconeogenesis, including glucose 6-phosphatas (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK), in the liver. RPSE supplementation increased the phosphorylation of forkhead box protein O1 (FOXO1) and AMP-activated protein kinase (AMPK), which underlined the mechanism of the anti-diabetic effects of RPSE. Taken together, RPSE has the potential to improve glycemic control by repressing hepatic gluconeogenesis via the phosphorylation of FOXO1 and AMPK in ObD mice.
Highlights
Type 2 diabetes mellitus (T2DM) is a metabolic disease that is principally caused by impaired insulin signaling and the discontinuation of insulin production in severe cases [1,2]
These novel findings proved that red pepper seeds extract (RPSE) supplementation transcriptionally downregulated the expression of gluconeogenic genes and proteins, including phosphoenolpyruvate carboxykinase (PEPCK) and GP6Pase, in the liver of obese diabetes (ObD)
RPSE supplementation ameliorated the biomarkers of glycemic control, including fasting glucose, HbA1c, and insulin
Summary
Type 2 diabetes mellitus (T2DM) is a metabolic disease that is principally caused by impaired insulin signaling and the discontinuation of insulin production in severe cases [1,2]. T2DM is associated with serious complications, including dyslipidemia, retinopathy, neuropathy, kidney failure, and stroke [3]. The International Diabetes Federation estimated that approximately 415 million adults (age, 20–79 years) to have diabetes in 2015, and the number will rise up to 642 million by 2040 [4]. We need to focus on the concomitant rise of obesity and type 2 diabetes—obese diabetes (ObD). Obesity is an independent risk factor for developing T2DM; >90% of T2DM are overweight or obese [5]. It is profoundly established that the pathological mechanism of obesity, in particular insulin resistance, expedites the development of T2DM
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