Developmental origins of health and disease: Impact of paternal nutrition and lifestyle

Most epidemiological and experimental studies have focused on maternal influences on offspring’s health.The impact of maternal undernutrition,overnutrition,hypoxia,and stress is linked to adverse offspring outcomes across a range of systems including cardiometabolic,respiratory,endocrine,and reproduction among others.During the past decade,it has become evident that paternal environmental factors are also linked to the development of diseases in offspring.In this article,we aim to outline the current understanding of the impact of male health and environmental exposure on offspring development,health,and disease and explore the mechanisms underlying the paternal programming of offspring health.The available evidence suggests that poor paternal pre-conceptional nutrition and lifestyle,and advanced age can increase the risk of negative outcomes in offspring,via both direct(genetic/epigenetic)and indirect(maternal uterine environment)effects.Beginning at preconception,and during utero and the early life after birth,cells acquire an epigenetic memory of the early exposure which can be influential across the entire lifespan and program a child’s health.Potentially not only mothers but also fathers should be advised that maintaining a healthy diet and lifestyle is important to improve offspring health as well as the parental health status.However,the evidence is mostly based on animal studies,and well-designed human studies are urgently needed to verify findings from animal data.

Maternal inappropriate calcium intake aggravates dietary-induced obesity in male offspring by affecting the differentiation potential of mesenchymal stem cells

BACKGROUND The effects of inappropriate dietary calcium intake in early life on later obesity have not been fully elucidated.AIM To raise the mechanism of maternal calcium intake on the multi-differentiation potential of mesenchymal stem cells among their male offspring.METHODS 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 normalfat 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.RESULTS 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.CONCLUSION 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.