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)
Summary
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.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
