Abstract
The beneficial effect of vitamin D (VD) supplementation on body weight gain limitation and inflammation has been highlighted in primary prevention mice models, but the long-term effect of VD supplementation in tertiary prevention has never been reported in obesity models. The curative effect of VD supplementation on obesity and associated disorders was evaluated in high-fat- and high-sucrose (HFS)-fed mice. Morphological, histological, and molecular phenotype were characterized. The increased body mass and adiposity caused by HFS diet as well as fat cell hypertrophy and glucose homeostasis were not improved by VD supplementation. However, VD supplementation led to a decrease of HFS-induced inflammation in inguinal adipose tissue, characterized by a decreased expression of chemokine mRNA levels. Moreover, a protective effect of VD on HFS-induced hepatic steatosis was highlighted by a decrease of lipid droplets and a reduction of triglyceride accumulation in the liver. This result was associated with a significant decrease of gene expression coding for key enzymes involved in hepatic de novo lipogenesis and fatty acid oxidation. Altogether, our results show that VD supplementation could be of interest to blunt the adipose tissue inflammation and hepatic steatosis and could represent an interesting nutritional strategy to fight obesity-associated comorbidities.
Highlights
We investigated the effect of vitamin D (VD) supplementation for 15 weeks on obese
We highlighted that VD supplementation did not modify the obese phenotype, adiposity, and insulin resistance in the high-fat/high-sucrose diet group (HFS) mice, but exerted an anti-inflammatory effect on Inguinal White Adipose Tissue (iWAT) and an improvement of hepatic steatosis
The protocol implemented to generate obesity was a 10-week HFS diet, which led to a significant increase in the total body mass and adiposity index of mice and as expected was associated with hyperglycemia and insulin resistance
Summary
Obesity, defined by an excessive fat accumulation in adipocytes, results from an imbalance between energy intake and energy expenditure. It is caused by changes in food consumption behaviors and lifestyle [1,2]. Nowadays, according to the World Health Organization (WHO), over 1.9 billion adults are overweight and among them 650 million are obese [3]. This pathology is strongly related to metabolic disorders such as arterial hypertension, chronic low-grade inflammation, and insulin resistance that could lead to type 2 diabetes [4,5]. Obesity is strongly linked to ectopic fat accumulation, in the liver, contributing to an emergence of non-alcoholic fatty liver disease (NAFLD) [6]
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