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.
Methylphenidate (MPH) is the active ingredient in Ritalin, although effective in treating ofthe attention deficit hyperactivity disorder (ADHD), its neurostimulation action is attractiveamong students in order to increase the focus or improving student performance. In context ofthe Developmental Origins of Health and Disease (DOHaD) concept, states that insults incritical phases of development, as the peripubertal period, may program the organism todysfunctions in adulthood. The aim of this work was to investigate the impact of peripubertalMPH exposure on learning and retrograde memory in adult rats. Male Wistar rats wereexposed to MPH (5 mg/kg) from post-natal day (PN) 30 until PN60 (MPH). Control animalsreceived 0.9% saline (Sal). At PN60, learning was evaluated true 10 days in an eight-armelevated maze and at PN120 retrograde memory. At PN60, MPH group showed a delay of61% in the latency, an increase of 100% in the number of errors and 200% in the number ofrepetition errors when compared to the Sal group, until the day 5 of learning period (p=0.004).After the washout period, at PN120, the MPH group showed an increase of 37% in thelatency, 49% in the number of errors of reference and 600% in the number of repetition errorscompared with the Sal group (p=0.001, p=0.004 and p=0.01). Exposure to MPH duringperipubertal phase decreases learning and memory in adult male Wistar rats.
Sedentary lifestyle and consumption of high-calorie foods contribute to the development ofindividuals with risk factors for non-communicable diseases. Aerobic exercise is one of themain non-pharmacological strategies in this confrontation. This work aims to evaluate theeffects of moderate-intensity exercise (MIE) on biometric and metabolic parameters of adultmale Wistar rats, programmed for obesity during the lactation period. The litters werestandardized in 9 pups until the 3rd day of life, and later adjusted in Normal Litters (NL), andReduced Litters (SL). At 21 days, the offspring were weaned and divided into sedentary(SED) and exercised (EXE) groups, forming 4 experimental groups: NL-SED, NL-EXE, SL-SED and SL-EXE. EXE rats performed a moderate-intensity treadmill running protocol from30 to 60 years old. All groups were euthanized at 120 days. The results showed that the litterreduction made the animals heavier (p<0.0001), hyperphagic (p<0.001), greater mesenteric fatstock (p<0.0001), insulin resistant (p=0.0001) and glucose intolerant (p=0.0001), whencompared to equivalent controls. MIE promoted a reduction in body weight (p=0.001) andmesenteric fat (p<0.0001), better insulin sensitivity (p=0.01) and glucose tolerance (p=0.003).It is concluded, therefore, that MIE performed in adolescence attenuates the deleteriouseffects observed on body composition and glucose metabolism in adult animals, programmedearly for obesity.
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.
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.
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.
The current study investigate sound effects of low-protein diet (LP) during peripubertal periodto induce metabolic dysfunctions. In our study (CEUA 2910011021), 30 days-old Wistar malerats received LP (4% protein) and control rats were fed a 20.5% protein diet, for 60 days (NPgroup). Biometric parameters was taken and glucose, total and HDL-cholesterol, andtriglycerides were evaluated from plasma samples. Glycemia homeostasis was evaluated byOGTT and ITT, while hepatic parameters, including quantitative analysis of fat, triglyceridesand cholesterol in the liver was evaluated ex vivo. At 60 days, LP rats showed inferior bodymass (P=0.003), food intake (P=0.05), and nose-tail length (P=0.0001), compared to NP.Regarding biochemical assays, LP rats showed higher serum glucose (P=0.008); however,triglyceride (P=0.002), total cholesterol (P=0.02), and HDL levels (P<0.0001) were lower inLP animals compared to NP group. LP rats also had minor glucose tolerance (P=0.02) andgreater insulin sensitivity (P=0.01). In the hepatic parameters, LP rats showed an increase inliver fat (P<0.0001), hepatic triglycerides (P<0.0001), cholesterol (P<0.0001), and liverweight (P<0.0001). Considering the present data, peripuberty protein restriction inducedmetabolic and hepatic dysfunctions at the end of puberty. Therefore, malnourished adolescentanimals are at higher risk of developing metabolic syndrome in adulthood.
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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