Published online Oct 26, 2022. doi: 10.4252/wjsc.v14.i10.756
Peer-review started: May 5, 2022
First decision: June 11, 2022
Revised: June 24, 2022
Accepted: August 7, 2022
Article in press: August 7, 2022
Published online: October 26, 2022
Processing time: 173 Days and 1.4 Hours
The effects of inappropriate dietary calcium intake in early life on later obesity have not been fully elucidated.
To raise the mechanism of maternal calcium intake on the multi-differentiation potential of mesenchymal stem cells among their male offspring.
Four-week-old female C57BL/6N mice were fed by deficient, low, normal and excessive calcium reproductive diets throughout pregnancy and lactation. Bone MSCs (BMSCs) were obtained from 7-day-old male offspring to measure the adipogenic differentiation potential by the Wnt/β-catenin signaling pathway. The other weaning male pups were fed a high-fat diet for 16 wk, along with normal-fat diet as the control. Then the serum was collected for the measurement of biochemical indicators. Meanwhile, the adipose tissues were excised to analyze the adipocyte sizes and inflammatory infiltration. And the target gene expressions on the adipogenic differentiation and Wnt/β-catenin signaling pathway in the adipose tissues and BMSCs were determined by real-time reverse transcription polymerase chain reaction.
Compared with the control group, maternal deficient, low and excessive calcium intake during pregnancy and lactation aggravated dietary-induced obesity, with larger adipocytes, more serious inflammatory infiltration and higher serum metabolism indicators by interfering with higher expressions of adipogenic differentiation (PPARγ, C/EBPα, Fabp4, LPL, Adiponectin, Resistin and/or Leptin) among their male offspring (P < 0.05). And there were significantly different expression of similar specific genes in the BMSCs to successfully polarize adipogenic differentiation and suppress osteogenic differentiation in vivo and in vitro, respectively (P < 0.05). Meanwhile, it was accompanied by more significant disorders on the expressions of Wnt/β-catenin signaling pathway both in BMSCs and adulthood adipose tissues among the offspring from maternal inappropriate dietary calcium intake groups.
Early-life abnormal dietary calcium intake might program the adipogenic differentiation potential of BMSCs from male offspring, with significant expressions on the Wnt/β-catenin signaling pathway to aggravate high-fat-diet-induced obesity in adulthood.
Core tip: Maternal inappropriate dietary calcium intake could aggravate high-fat-diet-induced obesity among male offspring, with larger adipocytes and more serious inflammatory infiltration by interfering with the higher expressions of adipogenic genes, which was accompanied by significant expressions of specific genes on the adipogenic and osteogenic differentiation. It was worsened by the disorders of Wnt/β-catenin signaling pathway both in the BMSCs and adipose tissues. So the importance of this study was that the prevention of adulthood obesity could be moved forward to the appropriate calcium intake in the neonatal period, even the formation of maternal germ cells and fertilized egg.