Ana Eliza Andreazzi

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.

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 β‐cells, which inhibit insulin secretion.

Protein restriction during lactation alters the autonomic nervous system control on glucose-induced insulin secretion in adult rats.

Abstract Involvement of autonomic nervous system (ANS) neurotransmitters on insulin secretion in rats submitted to protein malnutrition during lactation was studied. During the first 2/3 of lactation, mothers received a 4% protein diet (LP). Control group received normal diet (23% protein) (NP). After protein restriction, mothers received normal diets. At 81 days rats were submitted to intravenous glucose tolerance tests (ivGTT). Plasma glucose and insulin concentration (PIC) were measured. Glucose-induced insulin secretion (GIIS) was tested in pancreatic islets. Fasting normoglycemia and hypoinsulinemia were observed in LP rats. Glucose intolerance and low PIC in LP group were detected during ivGTT. Acetylcholine (Ach) or blockage of α-adrenoceptors induced high PIC increment in LP rats; atropine or stimulation of α-adrenoceptors did not change PIC. Insulin secretion of LP rat islets showed low glucose and carbachol responses. Epinephrine-inhibited GIIS in both islet groups. Hypoinsulinemia observed in lactation-malnourished rats might be caused by alterations in GIIS regulation, including ANS modulation.

Impaired Sympathoadrenal Axis Function Contributes to Enhanced Insulin Secretion in Prediabetic Obese Rats

The involvement of sympathoadrenal axis activity in obesity onset was investigated using the experimental model of treating neonatal rats with monosodium L-glutamate. To access general sympathetic nervous system activity, we recorded the firing rates of sympathetic superior cervical ganglion nerves in animals. Catecholamine content and secretion from isolated adrenal medulla were measured. Intravenous glucose tolerance test was performed, and isolated pancreatic islets were stimulated with glucose and adrenergic agonists. The nerve firing rate of obese rats was decreased compared to the rate for lean rats. Basal catecholamine secretion decreased whereas catecholamine secretion induced by carbachol, elevated extracellular potassium, and caffeine in the isolated adrenal medulla were all increased in obese rats compared to control. Both glucose intolerance and hyperinsulinaemia were observed in obese rats. Adrenaline strongly inhibited glucose-induced insulin secretion in obese animals. These findings suggest that low sympathoadrenal activity contributes to impaired glycaemic control in prediabetic obese rats.

Metabolic effects of exercise on childhood obesity: a current view

OBJECTIVE: To review the current literature concerning the effects of physical exercise on several metabolic variables related to childhood obesity. DATA SOURCE: A search was performed in Pubmed/MEDLINE and Web of Science databases. The keywords used were as follows: Obesity, Children Obesity, Childhood Obesity, Exercise and Physical Activity. The online search was based on studies published in English, from April 2010 to December 2013. DATA SYNTHESIS: Search queries returned 88,393 studies based on the aforementioned keywords; 4,561 studies were selected by crossing chosen keywords. After applying inclusion criteria, four studies were selected from 182 eligible titles. Most studies found that aerobic and resistance training improves body composition, lipid profile and metabolic and inflammatory status of obese children and adolescents; however, the magnitude of these effects is associated with the type, intensity and duration of practice. CONCLUSIONS: Regardless of the type, physical exercise promotes positive adaptations to childhood obesity, mainly acting to restore cellular and cardiovascular homeostasis, to improve body composition, and to activate metabolism; therefore, physical exercise acts as a co-factor in fighting obesity.

Behavior and memory evaluation of Wistar rats exposed to 1·8 GHz radiofrequency electromagnetic radiation

Abstract Background: The development of communication systems has brought great social and economic benefits to society. As mobile phone use has become widespread, concerns have emerged regarding the potential adverse effects of radiofrequency electromagnetic radiation (RF-EMR) used by these devices. Objective: To verify potential effects of mobile phone radiation on the central nervous system (CNS) in an animal model. Methods: Male Wistar rats (60 days old) were exposed to RF-EMR from a Global System for Mobile (GSM) cell phone (1·8 GHz) for 3 days. At the end of the exposure, the following behavioral tests were performed: open field and object recognition. Results: Our results showed that exposed animals did not present anxiety patterns or working memory impairment, but stress behavior actions were observed. Conclusion: Given the results of the present study, we speculate that RF-EMR does not promote CNS impairment, but suggest that it may lead to stressful behavioral patterns.

Altered behavior of adult obese rats by monosodium l-glutamate neonatal treatment is related to hypercorticosteronemia and activation of hypothalamic ERK1 and ERK2

Objectives: Obesity is a metabolic and hormonal disorder with serious social and psychological impacts. There is a close relationship among obesity, neuroendocrine homeostasis and behavioral patterns. However, few data are available in the literature regarding this subject. This study assessed behavior and memory of adult obese rats by monosodium l-glutamate (MSG) neonatal treatment or highly palatable dietary treatment. Methods: MSG obesity was induced by subcutaneous injections of MSG (4 mg/g) during the first 5 days of life (Ob-MSG); control group (C-MSG), received saline solution equimolar. Both groups were fed with commercial chow. To induce dietary obesity, 21-day-old rats were assigned to two experimental diets: highly palatable diet (Ob-Diet) and control diet (C-Diet) composed of commercial chow. Ninety-day-old animals were submitted to behavioral assessment by the open-field test and short- and long-term memory by the object recognition test. Biometric variables were obtained, the Lee index was calculated and mass of retroperitoneal and perigonadal fat pads was measured. Furthermore, an altered behavioral profile was investigated by quantification of plasmatic corticosterone, expression, and activity of hypothalamic extracellular signal-regulated kinase protein (ERK) 1 and 2. Results: Increased Lee index and fat pads were observed in Ob-MSG and Ob-Diet groups. Ob-MSG presented a higher level of anxiety and impaired long-term memory compared to C-MSG, while there was no difference between Ob-Diet and C-Diet. The Ob-MSG group presented a higher level of plasmatic corticosterone and increased phosphorylation of hypothalamic ERK1 and 2. Discussion: Both treatments induced obesity but only Ob-MSG showed altered behavioral parameters, which is related to increased concentration of corticosterone and hypothalamic ERK1 and 2 activation.

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.

Effects of moderate intensity endurance training vs. high intensity interval training on weight gain, cardiorespiratory capacity, and metabolic profile in postnatal overfed rats

BackgroundObesity is associated with several comorbidities, such as cardiovascular disease and type 2 diabetes mellitus, and may have its origin in early life stages, such as in the lactation period, through metabolic programming. Physical activity aids in decreasing the chances of developing cardiovascular and metabolic diseases, even with small weight losses and, in children, can play an essential role in preventing weight gain and other health problems. The present study aimed to evaluate the effects of moderate intensity endurance training and high intensity interval training (HIIT) protocols on obesity-related parameters and cardiorespiratory capacity in overfed Wistar rats throughout the breastfeeding period.MethodsTwo days after birth, forty male and female Wistar rats were clustered into two groups: Control Litter Group (CL; ten animals/litter) and Reduced Litter Group (RL; four animals/litter). At weaning, RL animals were distributed randomly into three experimental groups: sedentary, moderate intensity endurance training and HIIT, while CL animals were clustered into a sedentary group.ResultsRL male and female body weight, before weaning, was significantly higher when compared with CL animals. This difference was maintained between CLSed and RLSed groups after weaning during all assessed periods. Adiposity was significantly higher in RLSed males when compared to CLSed males, and alterations in glycaemic metabolism were also observed. Endurance and HIIT protocols were efficient in improving maximal cardiorespiratory capacity, as well as concerning the glycemic metabolism and central fat accumulation of males and females submitted to childhood overfeeding by the litter reduction method.ConclusionsBoth moderate endurance training and HIIT protocols included in early life were efficient in reverting or preventing certain metabolic alterations as a consequence of overfeeding during breastfeeding in male and female Wistar rats.