Research Article: Dietary calcium affects body composition and lipid metabolism in rats

Date Published: January 10, 2019

Publisher: Public Library of Science

Author(s): Haya Alomaim, Philip Griffin, Eleonora Swist, Louise J. Plouffe, Michelle Vandeloo, Isabelle Demonty, Ashok Kumar, Jesse Bertinato, Juan J. Loor.


Calcium (Ca) intakes may affect cardiovascular disease risk by altering body composition (body weight and fat) and serum lipid profile, but results have been inconsistent and the underlying mechanisms are not well understood. The effects of dietary Ca on body composition and lipid metabolism were examined in rats. Male Sprague-Dawley rats were fed high-fat, high-energy diets containing (g/kg) low (0.75Ca, 0.86 ± 0.05; 2Ca, 2.26 ± 0.02), normal (5Ca, 5.55 ± 0.08) or high (10Ca, 11.03 ± 0.17; 20Ca, 21.79 ± 0.15) Ca for 10 weeks. Rats fed the lowest Ca diet (0.75Ca) had lower (p < 0.05) body weight and fat mass compared to other groups. Rats fed the high Ca diets had lower serum total and LDL cholesterol compared to rats fed normal or low Ca. Liver total cholesterol was lower in rats fed high compared to low Ca. In general, liver mRNA expression of genes involved in cholesterol uptake from the circulation (Ldlr), cholesterol synthesis (Hmgcr and Hmgcs1), fatty acid oxidation (Cpt2) and cholesterol esterification (Acat2) were higher in rats fed higher Ca. Apparent digestibility of total trans, saturated, monounsaturated and polyunsaturated fatty acids was lower in rats fed the high compared to the low Ca diets, with the largest effects seen on trans and saturated fatty acids. Fecal excretion of cholesterol and total bile acids was highest in rats fed the highest Ca diet (20Ca). The results suggest little effect of dietary Ca on body composition unless Ca intakes are very low. Decreased bile acid reabsorption and reduced absorption of neutral sterols and saturated and trans fatty acids may contribute to the better serum lipid profile in rats fed higher Ca.

Partial Text

Calcium (Ca) is a mineral nutrient rich in milk products and plays an important role as a second messenger and in signal transduction [1]. Ca is essential for a vast number of physiological processes including bone metabolism, muscle function, nerve transmission, blood coagulation and hormone secretion. Serum ionized Ca concentrations are maintained within a narrow range through the concerted action of parathyroid hormone (PTH), 1,25-dihydroxyvitamin D and calcitonin that act at the intestine, kidneys and bone [2, 3].

Randomized controlled trials (RCT) and meta-analyses of RCT of Ca supplementation (with or without vitamin D) have reported a modest increase in risk of cardiovascular events, in particular myocardial infraction, in participants taking a Ca supplement (500–1000 mg/day) compared to placebo [12–14]. However, the totality of available evidence to date does not seem to support a causal inference between higher dietary Ca or Ca supplementation and increased risk of cardiovascular events [5, 62]. A recent updated systematic review and meta-analysis concluded that Ca intakes below the upper limit (i.e., 2000–2500 mg/day) were not associated with increased risk of CVD events or mortality in healthy adults [63]. Furthermore, there is some evidence suggesting that higher Ca intakes may lower CVD risk by promoting lower body weight or fat mass and positively altering serum lipid profile [6–11].

Ca intakes for a large segment of the North American population fall short of dietary recommendations [70, 71], while upper percentiles of intakes for some subpopulations (e.g., older women) exceed the upper limit from use of high-dose Ca supplements [72]. Thus, it is important to understand the effects of Ca intakes on CVD risk. This study has shown that differences in dietary Ca alone (i.e., without changes in other components in dairy foods) has little effect on body weight or fat mass in rats unless Ca intakes are very low. Diets containing above normal amounts of Ca induced changes in blood lipids predictive of a lower risk for CVD. More than one mechanism may account for the changes in blood lipids. At high Ca doses (20Ca diet containing ~400% of normal Ca), decreased absorption of neutral sterols and increased excretion of bile acids as well as decreased digestibility of TFA and SFA may have contributed to the lower serum TC and LDL-C. At a lower Ca dose above normal (10Ca diet containing ~200% of normal Ca), decreased digestibility of TFA and SFA may have played a larger role given the absence of a significant effect on cholesterol balance. Ca intakes of 200% normal requirements (i.e., ~2-fold the recommended dietary allowance) occur in the general population. Consumption of 400% normal Ca requirements is rare, but high concentrations of Ca in the GI tract can occur with consumption of high-dose Ca supplements at one time. A major finding reported in this paper is the large decrease in digestibility of TFA with higher dietary Ca. Further research is needed to determine whether the Ca in dairy products attenuates the adverse effects of TFA in these products. This is important since natural TFA may have the same adverse effects on blood lipids as industrial TFA, but are more difficult to remove from the food supply.




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