Abstract
In obesity, there is an accumulation of adipocytes which produces adipokine that are pro-inflammatory substance, such as leptin and MCP-1 and anti-inflammatory substance, such as adiponectin, while the bioavailability of vitamin D is decreased. This research aimed to study the effect of vitamin D administration on leptin, MCP-1, and adiponectin levels in adipose tissue rats with obesity. Vitamin D was administered to the obese model of 6-9 months old female Wistar rats. This experiment was a randomized control group design with a post-test group design only. Twenty-seven (27) female obese Wistar rats were included in this study. The animals were divided randomly into 3 groups: 9 rats were given 2400 IU vitamin D (group A), 9 rats were given 800 IU vitamin D (group B) and 9 rats were given a placebo as control (group C). The administration of Vitamin D was given once daily for 8 weeks. The visceral adipose tissue was taken to measure the level of leptin, adiponectin and mRNA MCP-1. Data among groups was analyzed by using one-way ANOVA and followed by LSD test, at a significance level of p <0.05. The lowest level of leptin (1059.15+135.20 pg/ml) and mRNA MCP-1 (2.36 + 0.75 fg/ml) and the highest adiponectin level (3.43 + 0.47 ng/ml) were found in group A. In conclusion, oral administration of vitamin D (2400 IU) decreased pro-inflammatory substances, such as leptin and mRNA MCP-1 and increased anti-inflammatory substances, such as adiponectin, in visceral adipose tissue of obese female Wistar rats.
Highlights
Obesity is caused by long-term imbalance of energy intake and usage
Vitamin D is an important target in adypocytes differentiation process, since it is predicted has a role in inhibiting or stimulating the expression of key molecules involved in differentiation, such as Wingless-related integration site (WNT), CAAT and Enhancer Binding Protein β (EBP)β
This research aimed to study the effect of vitamin D administration on leptin, mRNA Monocyte Chemoattractant Protein-1 (MCP-1) and adiponectin levels in visceral adipose tissue on rats with obesity
Summary
Obesity is caused by long-term imbalance of energy intake and usage. It is a global pandemic all over the world and has been stated as the biggest chronic health problem in adults by World Health Organization.[1]. Leptin is a peptide produced by adipocyte which is a hormone that regulates body fat reserves and it is related to adipose tissue This hormone is involved in energy balance homeostasis through central regulation, especially in fat accumulation and metabolic disorder. Many studies have shown a negative correlations between obesity and serum vitamin D levels, the causes and effects are still unclear.[12] Subjects with hypovitaminosis vitamin D have higher risk of developing metabolic disorders compared to ones without it.[13] Vitamin D is an important target in adypocytes differentiation process, since it is predicted has a role in inhibiting or stimulating the expression of key molecules involved in differentiation, such as Wingless-related integration site (WNT), CAAT (distinct pattern of nucleotides) and Enhancer Binding Protein β (EBP)β. This research aimed to study the effect of vitamin D administration on leptin, mRNA MCP-1 and adiponectin levels in visceral adipose tissue on rats with obesity
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