Abstract
Papain is a proteolytic enzyme present in the leaves, fruits, roots, and latex of the Carica papaya (papaya) plant. Although it exhibits a wide range of activities, there are no reports on the anti-obesity effects of papain. This study examined the anti-obesity effect and obesity-involved anti-inflammatory mechanism of papain in in vivo and in vitro models using high-fat diet (HFD)-induced obese mice and 3T3-L1 preadipocytes. Oral administration of papain reduced HFD-induced weight of the body, liver, and adipose tissues of mice. Papain also reduced hepatic lipid accumulation and adipocyte size. Moreover, serum total cholesterol and triglyceride levels were markedly reduced in papain-treated mice. In addition, papain inhibited the differentiation of preadipocytes and oil accumulation in 3T3-L1 preadipocytes and rat primary preadipocytes. Mechanistically, papain significantly downregulated the protein levels of key adipogenesis regulators and reversed the expression of pro-inflammatory cytokines and adipokines in HFD-induced obese mice and 3T3-L1 preadipocytes. Papain also markedly enhanced activation of the AMP-activated protein kinase pathway in both models. Collectively, these results suggest that papain exerts anti-obesity effects in HFD-induced mice and 3T3-L1 preadipocytes by regulating levels of adipogenic factors involved in lipid metabolism and inflammation; thus, it could be useful in the prevention and treatment of obesity.
Highlights
Obesity is a major risk factor that contributes toward a number of chronic diseases, including diabetes, hypertension, hyperlipidemia, cardiovascular diseases, and cancer with its prevalence increasing to epidemic proportions in recent decades [1]
In the condition of over-nutrition and obesity, the altered lipid metabolism leads to the accumulation of triglycerides in the liver through adipogenesis and lipogenesis, and to a clinical condition known as non-alcoholic fatty liver disease (NAFLD) [32]
Papain treatment noticeably suppressed the increased expression levels of adipogenesis-related transcription factors, including peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/EBPα), and sterol regulatory element-binding protein (SREBP)-1, in the liver induced by high-fat diet (HFD) feeding and MDI-treated 3T3-L1 preadipocytes (Figures 3 and 7)
Summary
Obesity is a major risk factor that contributes toward a number of chronic diseases, including diabetes, hypertension, hyperlipidemia, cardiovascular diseases, and cancer with its prevalence increasing to epidemic proportions in recent decades [1]. C/EBPs play an important role in activating PPARγ expression during the early stages of differentiation [6], PPARγ promotes lipogenic gene expression, and SREBP-1 induces fatty acid synthesis, such as acetyl-CoA carboxylase and fatty acid synthase [7]. As a strong risk factor for many diseases, obesity predisposes the body to a pro-inflammatory state via increased levels of inflammatory mediators such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, leptin, and reduced levels of adiponectin secreted by adipose tissue. This family of cytokines and hormones are collectively referred to as adipokines. AMPK is a molecular target of drugs used in the treatment of metabolic diseases, including obesity
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