Effects of pre- and early postnatal protein malnutrition on carcass composition and lipoprotein lipase activity in male rats

Abstract

Little is known about the effects of pre- and early postnatal protein malnutrition on energy storage (e.g., carcass lipid) and expenditure (e.g., brown adipose tissue [BAT] thermogenesis) and their reversibility by nutritional rehabilitation. Therefore, the purpose of these experiments was to examine the permanence of prenatal and early postnatal protein malnutrition on energy balance in rats. Five weeks before mating and through gestation adult female rats were fed either a 25 or 8% casein diet (designated 25 or 8). Diet reversals were performed at birth and/or weaning (designated B or W) and the pups were cross-fostered at birth. Thus, the groups were: (1) 25-25B (controls), (2) 8–25W (gestational and lactational protein malnutrition, (3) 82–5B (gestational protein malnutrition), and (4) 25-8B-25W (lactational protein malnutrition). Animals were weighed and sacrificed 200–250 days postpartum for carcass composition. Retroperitoneal white adipose tissue (RWAT) and interscapular BAT (IBAT) wet weights and lipoprotein lipase (LPL) activity were also measured in the 25-25B and 8–25W groups. Nutritional rehabilitation at birth (8–25B) resulted in normal body weights as adults. Lactational protein malnutrition (25-8B-25W) resulted in intermediate body weights to the controls (25-25W), which had the greatest weights, and the 8–25W group, which had the lowest weights. The 8–25W and 25-8B-25W rats also had significantly decreased carcass wet weight and total body water, fat and fat-free dry mass relative to the 25-25B and 8–25B groups, the latter two of which did not differ in their carcass composition. The 8–25B and 25-8B-25W groups exhibited a selective decrease in the percent of the carcass as lipid. Despite more than 6 months of nutritional rehabilitation beginning at weaning (8–25W), IBAT wet weight, total protein, and specific LPL activity (LPL activity per mg protein) were decreased relative to the 25-25B rats. Total IBAT LPL activity did not differ between the groups. Similarly, the 8–25W rats had decreased RWAT wet weight and total RWAT LPL activity relative to the 25-25B group. The critical time period for protein malnutrition to affect the mechanisms underlying the decreases in body mass and carcass lipid content may be during lactation, since the offspring of prenatally protein malnourished rats cross-fostered at birth to mothers fed a nutritionally adequate protein diet (8–25B) did not exhibit the selective decrease in carcass lipid content, but the offspring of gestational and lactational protein malnourished mothers (8–25W), and, more importantly, the offspring of lactationally protein malnourished mothers (25-8B-25W), both had decreased body weights and carcass lipid content despite the extended nutritional rehabilitation.