Sugared water consumption by adult offspring of mothers fed a protein-restricted diet during pregnancy results in increased offspring adiposity: the second hit effect

Abstract

Poor maternal nutrition predisposes offspring to metabolic disease. This predisposition is modified by various postnatal factors. We hypothesised that coupled to the initial effects of developmental programming due to a maternal low-protein diet, a second hit resulting from increased offspring postnatal sugar consumption would lead to additional changes in metabolism and adipose tissue function. The objective of the present study was to determine the effects of sugared water consumption (5 % sucrose in the drinking-water) on adult offspring adiposity as a 'second hit' following exposure to maternal protein restriction during pregnancy. We studied four offspring groups: (1) offspring of mothers fed the control diet (C); (2) offspring of mothers fed the restricted protein diet (R); (3) offspring of control mothers that drank sugared water (C-S); (4) offspring of restricted mothers that drank sugared water (R-S). Maternal diet in pregnancy was considered the first factor and sugared water consumption as the second factor -the second hit. Body weight and total energy consumption, before and after sugared water consumption, were similar in all the groups. Sugared water consumption increased TAG, insulin and cholesterol concentrations in both the sexes of the C-S and R-S offspring. Sugared water consumption increased leptin concentrations in the R-S females and males but not in the R offspring. There was also an interaction between sugared water and maternal diet in males. Sugared water consumption increased adipocyte size and adiposity index in both females and males, but the interaction with maternal diet was observed only in females. Adiposity index and plasma leptin concentrations were positively correlated in both the sexes. The present study shows that a second hit during adulthood can amplify the effects of higher adiposity arising due to poor maternal pregnancy diet in an offspring sex dependent fashion.

Paternal obesity induces metabolic and sperm disturbances in male offspring that are exacerbated by their exposure to an “obesogenic” diet

“…Interestingly Cervantes‐Rodriguez et al. () report a similar phenotype in their offspring (increased triglycerides, insulin, cholesterol, leptin, and adiposity) due to a second‐hit of sugar consumption following the first hit of maternal protein restriction. In this case the offspring phenotype due to maternal protein restriction was exacerbated by the consumption of 5% sucrose in drinking water beyond the individual effects seen for either being born to a protein restricted mother or the consumption of the sugar water alone (Cervantes‐Rodriguez et al.…”

“…; Cervantes‐Rodriguez et al. ). Using an Agouti mouse model of natural maternal obesity and diabetes with age Li et al.…”

“…In this case the offspring phenotype due to maternal protein restriction was exacerbated by the consumption of 5% sucrose in drinking water beyond the individual effects seen for either being born to a protein restricted mother or the consumption of the sugar water alone (Cervantes‐Rodriguez et al. ). Here, we report a similar phenomenon, with the male offspring phenotype worsened by the second‐hit of the consumption of a HFD with the “first‐hit” resulting from preconception paternal obesity/HFD.…”

Hypothyroidism Reduces the Size of Ovarian Follicles and Promotes Hypertrophy of Periovarian Fat with Infiltration of Macrophages in Adult Rabbits

“…Serum leptin concentrations were measured by RIA using commercial kits obtained from Linco Research, Inc. (Cat. number RL-83K) [20]. …”

Synergetic Effects of Prenatal and Postnatal High Sucrose Intake on Glucose Tolerance and Hepatic Insulin Resistance in Rat Offspring

“…For instance, offspring fed 70% of total calories as sucrose had a higher adiponectin concentration, and offspring fed 5% sucrose for 10 weeks presented with increases in adipocyte size and the adiposity index. However, other studies have revealed that affected offspring exhibit adaptive responses to abnormal prenatal exposures . The relationship between prenatal and postnatal high sucrose exposure and the possible mechanisms underlying this relationship are unclear.…”