Swimming training reduces glucose‐amplifying pathway and cholinergic responses in islets from lean‐ and MSG‐obese rats

Abstract

Here, we investigate the effects of exercise training on glucose‐ and cholinergic‐induced insulin secretion in pancreatic islets from obese and lean rats. Male Wistar rats were treated with monosodium glutamate (MSG) for the first 5 days of life, while control (CON) rats received saline. At 21 days, the rats were divided into exercised (EXE) and sedentary (SED) groups. The EXE rats swam for 30 minutes, three times/week, for 10 weeks. After this, MSG‐SED rats showed hyperglycaemia, hypertriglyceridaemia and hyperinsulinaemia. Besides, islets from MSG‐SED rats exhibited increased glucose‐stimulated insulin secretion (GSIS), followed by impaired glucose sensitivity, absence of glucose‐amplifying pathway and weak cholinergic response. In contrast, adiposity, hyperinsulinaemia and hypertriglyceridaemia were reduced in MSG‐EXE rats. Moreover, islets from MSG‐EXE rats exhibited lower GSIS and improved islet glucose sensitivity, without restoration of the glucose‐amplifying pathway or alteration in the weak cholinergic effect of these islets. In islets from CON‐EXE rats we also observed reduced GSIS and absence of glucose‐amplifying effects and an accentuated reduction in cholinergic insulinotropic responses, without effect on glucose sensitivity in pancreatic islets from this group. Neither obesity nor exercise modified Muscarinic Receptor 3 (M3R) immunocontent or its downstream pathways (PKC and PKA). Moreover, only CON‐EXE showed increased GSIS in the presence of calcium blocker, Thapsigargin. In conclusion, swimming training reduces GSIS and cholinergic responsiveness in isolated pancreatic islets from lean and hypothalamic obese rats, which could be due to the inhibition of glucose‐amplifying pathways.

Whole-Body Vibration Promotes Beneficial Changes on the Anterior Tibial Muscle Histomorphometry of Hypothalamic Obese Rats

“…Also, CTL animals increased nuclear activity, which may indicate the effect of exercise on protein synthesis. The MSG-induced obesity model promoted an increase in the Lee index, as well as the deposition of retroperitoneal and perigonadal body fats, that corroborates with studies which, that have already demonstrated a significant increase in these parameters and, therefore, the efficiency of the model for the induction of obesity in rats (14,15). The effectiveness of this experimental model is justified by the injuries that occur in several central structures in the paraventricular region, with the arcuate and ventromedial nuclei of the hypothalamus being the most affected sites, with 80% to 90% of the neurons responsible for controlling energy expenditure, food consumption and glycemic homeostasis (16).…”

Peripubertal Exposure to Glyphosate-Based Herbicides Promotes Histopathological Impairment in the Structure of the Diaphragm Muscle of c57bl/6 Mice

“…Then, laparotomy was performed to collect the organs. Retroperitoneal and peritoneal fat were collected and weighed and standardized by body weight (Borck et al 2020).…”

Early and Sustained Inflammatory State Induces Muscle Changes and Establishes Obesogenic Characteristics in Wistar Rats Exposed to MSG-Induced Obesity Model

“…The animals were then desensitized in a carbon dioxide chamber and then euthanized by decapitation [7]. Retroperitoneal, Perigonadal, and brown fats were removed, weighed, normalized to g.100 g − 1 of body weight, and used to calculate body adiposity [2]. Blood was collected in heparinized tubes and centrifuged at 4 °C, at 12,000 RCF (g) for 10 min to measure the plasma biochemical profile.…”

“…The model of obesity induced by perinatal injections of monosodium glutamate is widely studied and known in the literature [1][2][3]. The main alteration determined in this model is the damage and cell death of neurons in the hypothalamic nuclei, mainly in the arcuate nucleus (ARC), where this neuronal loss impairs the signalling mediated by insulin and affects the energy balance of the organism [3][4][5][6].…”

“…Due to the hyperphagic characteristic of the MSG model [7], the excessive consumption of nutrients is associated with the energy imbalance promoted by the hypothalamic lesion. In this model, obesity is associated with the secretion of pro-inflammatory cytokines by adipose tissue, which leads to insulin resistance, stimulating cell damage and impairing metabolic homeostasis in adipose tissue, liver, pancreas, brain, and muscles [1,2,[8][9][10][11][12][13].…”