Abstract

This study investigated the anti-obesity effects of collagen peptide derived from skate skin on lipid metabolism in high-fat diet (HFD)-fed mice. All C57BL6/J male mice were fed a HFD with 60% kcal fat except for mice in the normal group which were fed a chow diet. The collagen-fed groups received collagen peptide (1050 Da) orally (100, 200, or 300 mg/kg body weight per day) by gavage, whereas the normal and control groups were given water (n = 9 per group). The body weight gain and visceral adipose tissue weight were lower in the collagen-fed groups than in the control group (p < 0.05). Plasma and hepatic lipid levels were significantly reduced by downregulating the hepatic protein expression levels for fatty acid synthesis (sterol regulatory element binding protein-1 (SREBP-1), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC)) and cholesterol synthesis (SREBP-2 and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR)) and upregulating those for β-oxidation (peroxisome proliferator-activated receptor alpha (PPAR-α) and carnitine palmitoyltransferase 1 (CPT1)) and synthesis of bile acid (cytochrome P450 family 7 subfamily A member 1 (CYP7A1)) (p < 0.05). In the collagen-fed groups, the hepatic protein expression level of phosphorylated 5′ adenosine monophosphate-activated protein kinase (p-AMPK) and plasma adiponectin levels were higher, and the leptin level was lower (p < 0.05). Histological analysis revealed that collagen treatment suppressed hepatic lipid accumulation and reduced the lipid droplet size in the adipose tissue. These effects were increased in a dose-dependent manner. The findings indicated that skate collagen peptide has anti-obesity effects through suppression of fat accumulation and regulation of lipid metabolism.

Highlights

  • Obesity is characterized by an abnormal accumulation of body fat that contributes to the etiologies of various metabolic disorders including dyslipidemia, hepatic steatosis, insulin resistance, and type 2 diabetes mellitus [1]

  • Hyperlipidemia is induced by the dysregulation of hepatic lipid metabolism, which upregulates the synthesis of triglyceride (TG) and cholesterol and downregulates fatty acid oxidation [1]

  • Adipose tissue weights were higher in the high-fat diet (HFD)-fed groups (Figure 1D–F)

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Summary

Introduction

Obesity is characterized by an abnormal accumulation of body fat that contributes to the etiologies of various metabolic disorders including dyslipidemia, hepatic steatosis, insulin resistance, and type 2 diabetes mellitus [1]. Obese individuals have high central adiposity due to the accumulation of visceral adipose tissue, which may be linked to a significantly increased risk of hepatic steatosis. The increased flux of non-esterified free fatty acid (NEFA) from the visceral fat to the liver is one of the suggested underlying mechanisms [2]. Hyperlipidemia is induced by the dysregulation of hepatic lipid metabolism, which upregulates the synthesis of triglyceride (TG) and cholesterol and downregulates fatty acid oxidation [1]. These metabolic reactions could accelerate fat accumulation in the liver and exacerbate hepatic steatosis.

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