Abstract
Objective: Emerging evidence established the role of dietary calcium in the modulation of obesity. Obesity is known to induce inflammatory and oxidative stress in adipocytes resulting in several metabolic complications. In the present study, we evaluated the role of low and high calcium diet on systemic inflammatory response and oxidative stress markers in both plasma and hepatic tissues in male rats.
 Methods: A total of 30 male rats were divided into three groups and fed with control, low calcium (0.25%), and high calcium (1.0%) diet for 3 months. All the diets were isocaloric in nature. At the end of the treatment, all rats were sacrificed, followed by collection of blood and hepatic tissue for inflammatory, oxidative, antioxidant, and histological study.
 Results: Rats fed with a low calcium diet showed a significant increase in the body weight gain, liver mass, plasma inflammatory markers C-reactive protein, interleukin-6, and tumor necrosis factor-alpha. Low calcium diet significantly increased the lipid peroxidation and protein carbonylation and decreased the superoxide dismutase and glutathione peroxidase activities in both plasma and liver. High calcium diet, on the other hand, showed the reversed effect.
 Conclusion: Low calcium in the diet, along with obesity, increases the systemic inflammatory response, which in turn increases oxidative stress both in blood and hepatic tissues. This might be associated with obesity-induced hepatic disorder. High calcium in diet attenuates this effect.
Highlights
Within the past few years, the structure of dietary intake and the prevalence of obesity around the developing world have been changing at a rapid pace [1]
Several recent studies have identified that there exists an inverse relationship between dietary calcium intake and the mass of adipose tissue or body fat content, which in turn modulate the risk of obesity [3]
The increase in secretion of inflammatory markers such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) and decrease in secretion of adiponectin found to be associated with insulin resistance (IR), inflammation and oxidative stress in the liver
Summary
Within the past few years, the structure of dietary intake and the prevalence of obesity around the developing world have been changing at a rapid pace [1]. The excess accumulation of adipose tissue leads to adipocyte hypertrophy where the size of the adipocytes grows in size to accumulate the excess amount of triglycerides These hypertrophic adipocytes play a key role behind the onset of several metabolic dysfunctions such as IR, non-alcoholic fatty liver (NAFL), and cardiovascular diseases by altering the adipokine secretions [6,7]. The increase in secretion of inflammatory markers such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) and decrease in secretion of adiponectin found to be associated with IR, inflammation and oxidative stress in the liver These adipose-derived inflammatory molecules can induce the production of reactive oxygen species (ROS), which can promote lipid peroxidation leading to liver damage along with the decrease in hepatocyte antioxidants levels [8]. Adipose tissue-derived inflammatory markers seemed to regulate oxidative stress in other metabolically active organs like liver, which in turn increases the consequences of future metabolic complications
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