Effect of postnatal overfeeding on the male and female Wistar rat reproductive parameters.

Overweight/obesity has become a worldwide epidemic, and factors such as a sedentary lifestyle and inadequate eating habits directly contribute to the development of this condition. Studies indicate that rapid weight gain at critical development stages, such as the lactation period, is associated with the development of obesity, cardiovascular diseases, and diabetes in the long term. In addition to metabolic changes during adulthood, overweight/obesity may influence reproductive function of the population. In this context, the present study aimed to evaluate postnatal overfeeding effects on male and female Wistar rat reproductive parameters. Postnatal overfeeding was induced by applying the litter reduction method for both sexes. Forty animals were used, divided into four groups: two with normal litters (NL♂ and NL♀) and two with small litters (SL♂ and SL♀). The males were euthanized at 90 days of age, on the same date the females were mated. Females were also euthanized after the 20-day gestation. Metabolic and reproductive variables were analyzed. Regarding males, SL animals showed increased body weight, adiposity, and decreased relative weight of the seminal vesicle, prostate, and epididymis as well as changes in the ITT and OGTT glycemic tests. Concerning females, SL animals presented increased body weight, relative perigonadal fat weight, glucose intolerance as well as modify the vaginal opening and increased weight of female pup. The litter reduction method was efficient in leading to metabolic and reproductive alterations in male and female Wistar rat.

Childhood obesity: a (re) programming disease?

The aim of our article was to review the current literature on the effects of metabolic (re) programming on childhood obesity. PubMed/MEDLINE was the data source used to track the studies. Descriptors applied: children obesity, epigenetic, metabolic programming, exercise and nutrition. The focus was to analyze and discuss the international findings on the theme. The gathering of the papers was performed between June and August 2014. The search of articles with the descriptors used found 33.054 studies. In all, 5.709 studies were selected by crossing chosen keywords. Among these, after careful reading of the titles, 712 papers were considered potential as references. After applying inclusion/exclusion criteria, 50 studies were selected from 132 eligible abstracts. Most studies linked the development and treatment of obesity from epigenetically stimulated metabolic programming during the early stages of pregnancy and life. This review provides theoretical basis to the understanding that the programmed development of childhood obesity may be linked to early exposure to environmental factors, such as (nutrition and regular practice of exercise) and stimulus can epigenetically alter the modulation of the obesogenic metabolic behavior during pregnancy and the developmental stages of children and/or postpone the pathophysiologic disease stage to adulthood.

Metabolic imprinting by maternal protein malnourishment impairs vagal activity in adult rats.

Protein restriction during lactation has been suggested to diminish parasympathetic activity, whereas sympathetic activity is enhanced in adult rats. The present study analyses whether dysfunction of the autonomic nervous system is involved in the impairment of insulin secretion from perinatally undernourished rats. Male neonates were reared by mothers fed a low- (4%) protein (LP group) or normal- (23%) protein diet (NP group). At 81 days of age, LP rats showed less body mass than NP rats (318 ± 4 g versus 370 ± 5 g) (P < 0.001). Fat tissue accumulation decreased in LP [0.8 ± 0.03 g/100 g body weight (BW)] compared to NP rats (1.1 ± 0.04 g/100 g BW) (P < 0.001). LP were glucose-intolerant as registered by the area under the curve of an i.v. glucose tolerance test (37 ± 3) compared to NP rats (29 ± 2) (P < 0.05); however, LP animals showed fasting normoglycaemia (LP, 5.0 ± 0.1; NP, 4.9 ± 0.03 mm) and hypoinsulinaemia (LP, 0.10 ± 0.02 ng/ml; NP, 0.17 ± 0.02 ng/ml). LP also showed glucose tissue uptake 60% higher than NP rats (P < 0.05). Vagus firing rate from LP was lower (7.1 ± 0.8 spikes/5 s) than that in NP rats (12.3 ± 0.7 spikes/5 s) (P < 0.001); however, there was no difference in sympathetic nervous activity. The cholinergic insulinotrophic effect was lower in pancreatic islets from LP (0.07 ± 0.01 ng/min/islet) than in NP rats (0.3 ± 0.06 ng/min/islet), whereas the levels of adrenaline-mediated inhibition of glucose-induced insulin release were similar. Perinatal protein restriction inhibited the activity of the vagus nerve, thus reducing the insulinotrophic effect of parasympathetic pathways on pancreatic ß-cells, which inhibit insulin secretion.

Swimming exercise at weaning improves glycemic control and inhibits the onset of monosodium L-glutamate-obesity in mice.

Swimming exercises by weaning pups inhibited hypothalamic obesity onset and recovered sympathoadrenal axis activity, but this was not observed when exercise training was applied to young adult mice. However, the mechanisms producing this improved metabolism are still not fully understood. Low-intensity swimming training started at an early age and was undertaken to observe glycemic control in hypothalamic-obese mice produced by neonatal treatment with monosodium l-glutamate (MSG). Whereas MSG and control mice swam for 15 min/day, 3 days a week, from the weaning stage up to 90 days old, sedentary MSG and normal mice did not exercise at all. After 14 h of fasting, animals were killed at 90 days of age. Perigonadal fat accumulation was measured to estimate obesity. Fasting blood glucose and insulin concentrations were also measured. Fresh isolated pancreatic islets were used to test glucose-induced insulin release and total catecholamine from the adrenal glands was measured. Mice were also submitted to intraperitoneal glucose tolerance test. MSG-obese mice showed fasting hyperglycemia, hyperinsulinemia, and glucose intolerance. Severe reduction of adrenal catecholamines content has also been reported. Besides, the inhibition of fat tissue accretion, exercise caused normalization of insulin blood levels and glycemic control. The pancreatic islets of obese mice, with impaired glucose-induced insulin secretion, were recovered after swimming exercises. Adrenal catecholamine content was increased by swimming. Results show that attenuation of MSG-hypothalamic obesity onset is caused, at least in part, by modulation of sympathoadrenal axis activity imposed by early exercise, which may be associated with subsequent glucose metabolism improvement.

Swim training applied at early age is critical to adrenal medulla catecholamine content and to attenuate monosodium L-glutamate-obesity onset in mice.

Exercise has been recommended as a remedy against a worldwide obesity epidemic; however, the onset of excessive weight gain is not fully understood, nor are the effects of exercise on body weight control. Activity deficits of the sympathetic nervous system, including the sympathoadrenal axis, have been suggested to contribute to high fat accumulation in obesity. In the present work, swim training was used to observe fat accumulation and adrenal catecholamine stocks in hypothalamic-obese mice produced by neonatal treatment with monosodium L-glutamate (MSG). MSG-treated and normal mice swam for 15 min/day, 3 days a week, from weaning up to 90 days old (EXE 21-90); from weaning up to 50 days old (EXE 21-50) and from 60 up to 90 days old (EXE 60-90). Sedentary MSG and normal mice (SED groups) did not exercise at all. Animals were sacrificed at 90 days of age. MSG treatment induced obesity, demonstrated by a 43.08% increase in epididymal fat pad weight; these adult obese mice presented 27.7% less catecholamine stocks in their adrenal glands than untreated mice (p<0.001). Exercise reduced fat accumulation and increased adrenal catecholamine content in EXE 21-90 groups. These effects were more pronounced in MSG-mice than in normal ones. Halting the exercise (EXE 21-50 groups) still changed fat accretion and catecholamine stocks; however, no effects were recorded in the EXE 60-90 groups. We conclude that metabolic changes imposed by early exercise, leading to an attenuation of MSG-hypothalamic obesity onset, are at least in part due to sympathoadrenal activity modulation.