Chronic maternal feed restriction impairs growth but increases adiposity of the fetal guinea pig

Abstract

Small size at birth has been associated with an increased risk of central obesity and reduced lean body mass in adult life. This study investigated the time of onset of prenatally induced obesity, which occurs after maternal feed restriction, in the guinea pig, a species that, like the human, develops substantial adipose tissue stores before birth. We examined the effect of maternal feed restriction [70% ad libitum intake from 4 wk before to midpregnancy, then 90% until day 60 gestation (term ∼69 days)] on fetal growth and body composition in the guinea pig. Maternal feed restriction reduced fetal (−39%) and placental (−30%) weight at 60 days gestation and reduced liver, biceps muscle, spleen, and thymus weights, relative to fetal weight, while relative weights of brain, lungs, and interscapular and retroperitoneal fat pads were increased. In the interscapular depot, maternal feed restriction decreased the volume density of multilocular fat and increased that of unilocular fat, resulting in an increased relative weight of interscapular unilocular fat. Maternal feed restriction did not alter the relative weight of perirenal fat or the volume density of adipocyte populations within the depot but increased unilocular lipid locule size. Maternal feed restriction in the guinea pig is associated with decreased weight of major organs, including liver and skeletal muscle, but increased adiposity of the fetus, with relative sparing of unilocular adipose tissue. If this early-onset obesity persists, it may contribute to the metabolic and cardiovascular dysfunction that these offspring of feed-restricted mothers develop as adults.

Brown adipose tissue genes in pericardial adipose tissue of newborn sheep are downregulated by maternal nutrient restriction in late gestation

“…In guinea pigs, maternal undernutrition increases the relative adiposity of the fetus and appears to preserve WAT at the expense of BAT in the interscapular depots (24). In sheep, maternal nutrient restriction in late gestation results in a 2.5-fold decrease in the abundance of UCP1 mRNA in near-term fetal adipose tissue, but there is no effect on protein abundance at this stage (6).…”

Maternal prenatal undernutrition alters the response of POMC neurons to energy status variation in adult male rat offspring

“…On the one hand, it has been shown that IUGR might be responsible for somatic growth alterations leading to shorter (body length) and lighter (body weight) rat offspring (21,25,53,55). Thus, in addition to skeletal growth modifications (16,21), we cannot rule out the possibility that a different lean-to-fat mass ratio due to a deficit in muscle mass and/or different body fat pad distribution occurs in adult FR30 rats (25). To address this question, further experiments, such as absorptiometric studies, are needed to measure the total body composition of FR30 adult rats.…”

Seminal fluid and reproduction: much more than previously thought

“…Foetal growth potential is controlled at many levels; however one very critical factor is that of the in utero maternal environment. Maternal feed restriction, through experimental approaches or food shortage, like that of the Dutch famine during World War II, has been correlated with low birth weight and subsequent changes in endocrine, metabolic and reproductive parameters in these offspring later in life, as well as predisposition to certain cancers [17][18][19][20][21][22][23][24][25][26]. It is hypothesised that these changes in endocrine and metabolic parameters are in essence programming the offspring for the development of endocrine associated adult diseases.…”