Immune modulation in the prevention of pathologies relating to diet-induced obesity

Non-alcoholic fatty liver disease (NAFLD) results from accumulation of fat in liver, so-called steatosis. Fatty liver may lead to the development of inflammation (steatohepatitis). This study analysed the role of high fat diet, Vitamin D, and complement properdin in mouse models of high fat diet. Properdin knockout mice, and properdin wild type mice on LDLR-/- and LDLR+/+ background were fed a high fat –high sugar diet or Western (high fat) diet. Body weight, fat pad weight, liver histopathology, immunohistochemistry were analysed. Hepatic expression of candidate genes (TNF-α, srebp-1c, TLR4, HMGCR, SR-B1, PPAR-y) was performed by qPCR. ELISA was used to quantify serum insulin, Adiponectin, MDA. Liver function test, endotoxin, complement activation, Western blot were evaluated. in vivo results showed that a high fat–high sugar diet and so-called Western diet led to the development steatosis, inflammation, and properdin has a role in the prevention of obesity, and metabolic syndrome diseases. Vitamin D given to mice fed high fat –high sugar diet led to the prevention of obesity, and associated complications. Exercising mice combined with supplemented Vitamin D had a better effect to prevent metabolic syndrome diseases. in vitro results shown that DHA, Vitamin D, and Allicin had anti-inflammatory roles by reducing TNF-α to LPS stimulation.