Abnormality in Maternal Dietary Calcium Intake During Pregnancy and Lactation Promotes Body Weight Gain by Affecting the Gut Microbiota in Mouse Offspring

Abstract

Scope To investigate the effects of calcium status in early life on adult body weight and the underlying mechanisms involved in gut microbiota and related lipid metabolism. Methods and results Three to four‐week‐old C57BL/6J female mice were fed diets with normal, insufficient, and excessive calcium respectively throughout pregnancy and lactation. The weaning male pups were fed with a high‐fat diet for 16 weeks, with a normal‐fat diet to the normal calcium group as control. The offspring fecal microbiota was analyzed by 16S rRNA high‐throughput sequencing, and mRNA expressions of genes were determined by the real‐time RT‐PCR. Maternal insufficient or excessive calcium intake exacerbated offspring obesity, with expressional changes in the Fasn, Acc1, LPL, Fiaf, and PPAR‐α genes in the liver or fat. The dysbiosis in gut microbiota in obese offspring was exacerbated by maternal imbalanced calcium intake, with increased Firmicutes and decreased Bacteroidetes in calcium insufficiency, and decreased Verrucomicrobia in calcium excess. Several genera, including Bacteroides, were reduced, and Lachnospiraceae and Lactobacillus were increased by maternal insufficient or excessive calcium intake. Conclusion Imbalance in maternal calcium intake promotes body weight gain in offspring, which may be mediated by calcium's modulation on the gut microbiota and lipid metabolism.

Calcium Oxalate Nephrolithiasis and Gut Microbiota: Not just a Gut-Kidney Axis. A Nutritional Perspective

“…However, one study conducted in mouse models of obesity has highlighted that the introduction of calcium supplementation could be associated with beneficial effects on the gut microbiota [125]. Reduced or excessive calcium intake could also influence the development of obesity through modulation of microbiota in weaning mouse pups [126]. Moreover, modulation of microbiota through prebiotic supplements can positively modulate dietary calcium absorption in mice, which represents a promising strategy for reducing the burden of hypercalciuria in kidney stone formers [127].…”

Alteration of gut microbiota affects expression of adiponectin and resistin through modifying DNA methylation in high-fat diet-induced obese mice

“…Co., Ltd., China). SCFAs in feces were examined using gas chromatography (GC) according to our previously described method [26] on an Agilent 6890N GC system equipped with a flame ionization detector (FID) and a highresolution gas chromatography column of 30 m × 0.25 mm i.d. coated with 1.40 μm film thickness (DB-624UI, J&W Scientific, Agilent Technologies Inc., USA).…”

Sex-specific maternal calcium requirements for the prevention of nonalcoholic fatty liver disease by altering the intestinal microbiota and lipid metabolism in the high-fat-diet-fed offspring mice

“…35 Our previous epidemiological and animal experiments have confirmed that maternal calcium intake could promote the growth and development of the infants, while imbalance in maternal calcium intake would aggravate the high-fat induced obesity of the adult male mouse offspring through modulating on the gut microbiota and lipid metabolism. 20 In addition, our animal study found that maternal insufficient or excessive calcium status during pregnancy and lactation programmed an abnormal expression of hepatic and adipose genes in the offspring, leading to dyslipidemia and hepatic lipid accumulation with the normal diets 36 In the current study, maternal inappropriate calcium supplementation has long-term effects on the progress of high-fat induced NAFLD among the mouse offspring by altering the intestinal microbiota and lipid metabolism. Specifically, maternal normal and low calcium intake could respectively have the greatest inhibition on the progress of NAFLD in the male and female mouse offspring, which was characterized by the least lipid droplets, inflammatory infiltration and fibrosis, the lowest concentrations of free fatty acids and triglycerides, the lowest expression of genes involving in de novo lipogenesis and the highest expression of genes related to lipolysis.…”

“…The histological analysis also showed the accumulation of lipid droplets, in the hepatic tissue was more heavier in the LC-HFD and HC-HFD groups than that in the NC-HFD group (P < .05). 20 The inflammation and fibrosis has been clearly shown in Figures 2 and 3. In the mice fed with the HFD, local inflammation and fibrosis were more serious than those in the NC-C group (Figures 2(a) (Figure 2(j)), and IL-10 (Figure 2(k)).…”

“…All the microbial data were analyzed on the free online platform of Majorbio I-Sanger Cloud Platform (www.i-sanger.com). 20 To clarify the similarities of intestinal flora composition among all the experimental groups (NC-C, NC-HFD, LC-HFD, and HC-HFD), the estimators of α-diversity (Shannon, Simpson, Ace and Chao indexes) were calculated based on rarefied OTU tables. Principal Coordinates Analyses (PCA) of unweighted UniFrac distance matrix is displayed as the β-diversity.…”