Low-protein diet in adult male rats has long-term effects on metabolism

Abstract

Nutritional insults during developmental plasticity have been linked with metabolic diseases such as diabetes in adulthood. We aimed to investigate whether a low-protein (LP) diet at the beginning of adulthood is able to program metabolic disruptions in rats. While control rats ate a normal-protein (23%; NP group) diet, treated rats were fed a LP (4%; LP group) diet from 60 to 90 days of age, after which an NP diet was supplied until they were 150 days old. Plasma levels of glucose and insulin, autonomous nervous system (ANS), and pancreatic islet function were then evaluated. Compared with the NP group, LP rats exhibited unchanged body weight and reduced food intake throughout the period of protein restriction; however, after the switch to the NP diet, hyperphagia of 10% (P!0.05), and catch-up growth of 113% (P!0.0001) were found. The LP rats showed hyperglycemia, insulin resistance, and higher fat accretion than the NP rats. While the sympathetic tonus from LP rats reduced by 28%, the vagus tonus increased by 21% (P!0.05). Compared with the islets from NP rats, the glucose insulinotropic effect as well as cholinergic and adrenergic actions was unaltered in the islets from LP rats. Protein restriction at the beginning of adulthood induced unbalanced ANS activity and fat tissue accretion later in life, even without functional disturbances in the pancreatic islets.

Anthropometry, Fatty Liver, Plasma Lipid, and Adipose Tissue on Rat Wistar Induced Low-Protein Diet

“…Both studies showed the decreasing food intake affects weight gain during the administration of low protein diet. Study from Malta et al and de Oliveira et al revealed, 30 days low protein diet on rat induces hyperleptinemia thus decreases food appetite on rat [11,12].…”

“…Malta et al and de Oliveira et al [11,12] reported that low protein diet (4% total energy) on rat decreased food intake compared to normal protein diet on a rat. The Impact of decreased intake in that research is similar to this research.…”

Protein-energy malnutrition at mid-adulthood does not imprint long-term metabolic consequences in male rats

“…Interestingly, even just after the pubertal phase (at beginning of adult life), rats supplied with the same low-protein diet display glucose-insulin homeostasis and ANS function alterations, without notably effects on pancreatic β-cells [18]. In light of these data, we surmise that the critical time windows involved in metabolic programming are not only restricted to early perinatal stages but that environmental factors that are applied during puberty or young adulthood may also have long-lasting metabolic consequences.…”

“…After these periods, rats are considered adult. However, some studies have used the term "young adulthood" or "early adulthood" from 60 to 90 days old or 4-6 months old [20,21], and the term "adult" from 90 days of age and onward [22]. Additionally, "old adult", from age 18-24 months or more, has also been used [23]; here, we refer to mid-adulthood rats with rats that are at least 90 days old.…”

“…Because metabolic malprogramming is supposed to be dependent upon the critical life development phases, such as the fetal [13,24], neonatal [24,25], pubertal [6,10,26] and early adulthood phases [18], where neuronal cell connections are vulnerable to injury and environmental insults that can imprint metabolic dysfunction, we assessed, in the present study, whether a low-protein diet that was administered to mid-adulthood rats (from 90 to 120 days of age) could also promote long-term metabolic dysfunctions.…”