Under- or overnutrition, during critical periods of development, lead to the development ofobesity and cardiometabolic dysfunction later in life in rats that have been programmed forthe development of metabolic dysfunction in a litter reduction model. On day 1, all litters arestandardized to 9 pups per dam and on day 3 after birth, litters were adjusted to 3 pups perdam in the small litter group (SL) and the NL group remained with 9 animals. At 70 days ofage, the animals were separated into 2 new groups: Saline (SAL) and Metformin (MET). For12 days, the NL and SL animals were treated daily with saline, giving rise to the NL-SAL andSL-SAL groups, or were treated with Met 100mg/kg/day, giving rise to the NL-MET and SL-MET groups. The treatment ended at 82 days of age and the animals were taken up to 142days of life. Body weight remained significantly higher in SL compared to NL animals up to142 days (p<0.0001), with no significant difference in relation to treatment. And the samewas observed in relation to glucose intolerance and insulin resistance (p<0.0001). We canconclude that short-term treatment with metformin did not attenuate the metabolicdysfunction induced by neonatal overnutrition.
Excess weight in adult life is an important risk factor for the development ofnoncommunicable diseases. On the other hand, aerobic physical exercise programs have beenshown to be important components both in the prevention and control of these conditions.This work aims to evaluate the effects of moderate intensity training on the body weight(BW) and food intake (FI) of adult male rats. Wistar rats were obtained at 30 days old.Throughout the experimental period, they were kept in appropriate cages (4 rats per box)containing food and water, temperature (22ºC) and photoperiod (07:00 to 19:00) controlled.At PN 40 they were divided into sedentary (S) and exercised (E) groups. The BW and FI weremeasured twice a week, from 40 to 140 days old. Exercised rats performed a moderate-intensity treadmill running from PN 90 to 120. During this period, they were submitted to aneffort test to evaluate performance and control the training load (55% to 65% VO 2max ). Theresults showed that both BW and FI were not altered with the training performed during adultlife, even after 20 days of exercise cessation. More studies are needed in order to assesswhether moderate-intensity training is able to attenuates the deleterious effects observed inthe biometric and metabolic markers of adult rats programmed for obesity and/or metabolicsyndrome.
Each stage (early, middle and late) of lactation is a critical period during which maternalmalnutritional can negatively effects on the offspring's body development. We investigatedthe effects of a maternal high fat diet (HF) during the different stages of lactation on bodyweight of male offspring at weaning. Female Wistar rats were fed either a HF diet only duringthe first week (HF1-7 group), second week (HF7-14 group), third week (HF14-21 group) andthroughout lactation (group HF1-21) or standard diet during all lactation. Biometricparameters of dams and male offspring were evaluated. HF fed dams did not have a differencein body weight, food intake and fat pad compared with the control dams. Regarding theoffspring, a higher final body weight was observed in males from the HF7-14 and HF14-21and HF21 groups compared to the control. There was an increase in retroperitoneal andmesenteric fat in HF21 and HF14-21 compared with control groups. Higher perigonadal fatpat was only observed in HF21. Consumption of maternal HF diet throughout lactation causeshigh body weight in male offspring. Interestingly, each isolated phase also causes importantbody weight accumulation, mainly the second and third week.
Regular consumption of dietary sugars can cause significant damage to the β-cells. Almost a century after the discovery of insulin, it has been suggested that the frequent consumption of certain carbohydrates can damage pancreatic β-cells, causing disturbances in the regulation of insulin secretion. Most noncommunicable diseases, such as diabetes, obesity, and hypertension have a common origin, metabolic dysfunction, which is partly due to β-cell malfunction. In this article, we believed that sugars can lead to an imbalance in cellular metabolism, causing insulin exocytosis to dangerously increase or decrease blood insulin concentrations. In this study, we describe the major mechanism of insulin secretion and discuss the effects of sugar on pancreatic β-cells. Although many environmental factors strongly influence β-cells, occidental diet, including excess sugar, has been found to be the predominant factor that kills or disrupts the functioning of the unique cells that produce, store, and secrete insulin.
Maternal nutritional insults during lactation can modulate the offspring phenotype associatedwith the risk of non-communicable diseases at different stages of ontogenetic development.The aim of this research was to analyze biometric and biochemical parameters of male Wistarrats, born to dams fed a low-protein diet in the first two-thirds of lactation. Therefore, themothers received ad libitum a normal (NP, 23%) or low-protein (LP, 4%) diet, originatingtwo experimental groups that were evaluated at 14 days old (NP-14 and LP-14). The resultsshowed that the LP-14 offspring male rats had lower body weight (p<0.0001), reduced liver(p<0.0001) and higher brown fat deposits (p<0.0001), compared to the equivalent control.They also exhibited hyperglycemia (p<0.05), hypercholesterolemia (p<0.0001), and increasedserum β-hydroxybutyrate (p<0.0001), contrasting with reduced triglycerides (p<0.05) levels.We conclude that maternal exposure to a low-protein diet during lactation was able toprogram 14-day-old male neonates to develop a metabolic syndrome phenotype, probably dueto restriction of body and visceral growth in these animals.
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