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Introduction: High‐fat diet (HFD) consumption and being exposed to daily psychological stress, common environmental factors in modern lifestyle, play an important role on metabolic disorders such as glucose homeostasis impairment. The aim of this study was to investigate the effects of high‐fat diet (HFD) and psychological stress combination on metabolic response to chronic psychological stress in male rats. Method: Male Wistar rats were divided into HFD, and normal diet (ND) groups and then into stress and nonstress subgroups. The diets were applied for 5 weeks, and psychological stress was induced for 7 consecutive days. Then, blood samples were taken to measure glucose, insulin, free fatty acids (FFA), and leptin and corticosterone concentrations. Subsequently, glucose‐stimulated insulin release from pancreatic isolated islets was assessed. Results: HFD did not significantly change fasting plasma glucose, insulin and corticosterone levels, whereas increased plasma leptin (7.05 ± 0.33) and FFA (p < 0.01) levels and impaired glucose tolerance. Additionally, HFD and stress combination induced more profound glucose intolerance associated with increased plasma corticosterone (p < 0.01) and leptin (8.63 ± 0.38) levels. However, insulin secretion from isolated islets did not change in the presence of high‐fat diet and/or stress. Conclusion: HFD should be considered as an intensified factor of metabolic impairments caused by chronic psychological stress. [ABSTRACT FROM AUTHOR]

Objective. Early life stress influences the development of metabolic disorders, including functional changes in the developing of pancreas mediated hypothalamic-pituitary-adrenal (HPA) axis. In the present study, the role of an early postnatal stress on corticosterone, glucose, and insulin levels was investigated during young adulthood.

Introduction: High-fat fructose diet (HFFr) consumption leads to inflammatory response and adverse metabolic consequences. Evaluating the changes in pancreatic-derived factor (PANDER) as one of the inflammatory metabolites, due to its regulatory role in glucose metabolism, could provide insight into the glucose homeostasis mechanisms. Methods: Dams and their pups were randomly assigned to a standard diet (StD) and HFFr groups. After weaning, the male Wistar offspring were allocated to StD, StD-DMSO (Vehicle: V), StD-4-phenyl butyric acid (Drug: D), HFFrD, HFFrD-V and HFFrD-D groups, while they were on their diet for five weeks and treated for ten days. At the end of the procedure, the plasma glucose, insulin and PANDER levels, atherogenic indices and pancreatic PANDER content were determined. Results: HFFrD intake increased plasma glucose level and homeostasis model assessment of insulin resistance. Also, atherogenic indices were elevated through the increase of cholesterol and low-density lipoprotein and the decrease of high-density lipoprotein (HDL) in HFFrD group. An increase in both plasma and pancreatic PANDER levels was observed in the HFFrD group. The drug decreased the plasma and pancreatic PANDER levels along with plasma glucose, cholesterol and the ratio of cholesterol to HDL levels in the HFFrD group. Conclusion: Since long-term HFFrD intake led to hyperglycemia, insulin resistance and dyslipidemia with an increase in plasma and pancreatic PANDER levels, and on the other hand, 4-phenyl butyric acid administration decreased PANDER levels as well as plasma glucose and cholesterol concentrations, PANDER increment may be the cause of glucose and lipid disturbances. [ABSTRACT FROM AUTHOR]

Introduction: Given the suggested metabolic regulatory effects of stress-responsive genes and based on the impacts of early-life stress on HPA axis development, this study aimed to characterize the maternal separation (MS) impact on the communication between glucose metabolism and HPA axis dysregulations under chronic social defeat stress (CSDS). Methods: During the first 2 weeks of life, male Wistar rats were either exposed to MS or left undisturbed with their mothers (Std). Starting on postnatal day 50, the animals of each group were either left undisturbed in the standard group housing (Con) or underwent CSDS for 3 weeks. There were four groups (n = 10/group): Std-Con, MS-Con, Std-CSDS, and MS-CSDS. Results: Early and/or adult life adversity reduced β-cell number, muscular FK506-binding protein 51 (FKBP51) content, and BMI in adulthood. The reduction of β-cell number and BMI in the MS-CSDS rats were more profound than MS-Con group. CSDS either alone or in combination with MS reduced locomotor activity and increased and decreased corticotropin-releasing factor type 1 receptor (CRFR1) content, respectively, in hypothalamus and pancreas. Although, under CSDS, MS intensified HPA axis overactivity and reduced isolated islets' insulin secretion, it could promote resilience to depression symptoms. No differences were observed in hypothalamic Fkbp5 gene DNA methylation and glucose tolerance among groups. Conclusion: MS exacerbated HPA axis overactivity and the endocrine pancreas dysfunctions under CSDS. The intensified corticosterone secretion and the diminished content of pancreatic CRFR1 protein could be involved in the reduced β-cell number and islets' insulin secretion under CSDS. The decreased muscular FKBP51 content might be a homeostatic response to slow down insulin resistance development under chronic stress. [ABSTRACT FROM AUTHOR]

This study investigated the effect of long-term high-fat diet (HFD) on plasma lipid profile and probability of inflammation in adult rats. After weaning, male offspring were divided into six groups based on diet type and medication. After 20 weeks of dietary intake, 4-PBA (endoplasmic reticulum (ER) stress inhibitor) was injected for three days. Then, blood samples were taken to measure plasma concentrations of low-density lipoprotein (LDL), triglyceride (TG), high-density lipoprotein (HDL), cholesterol, leptin and interleukin 1-β (IL 1-β). The HFD increased body weight and food intake and intra-abdominal fat and thymus weights, which were associated with elevated plasma leptin level. Moreover, HFD increased plasma concentrations of TG, LDL, cholesterol and IL 1-β and decreased HDL level. Injection of 4-PBA reversed the plasma parameters changes caused by HFD. It seems that long-term HFD feeding through inducing the ER stress, disrupted the lipid metabolism and resulted in inflammation. [ABSTRACT FROM AUTHOR]

This study examined foot shock stress effects, during weaning, on pancreatic HB9 protein expression in young adult male rats in the presence or absence of adulthood stress. The pups were divided into Control, Early life stress, Young adult stress, and Early + young adult stress groups. Plasma corticosterone, insulin, glucose, and TNF-α concentrations, and pancreatic HB9 protein expression were assessed. At 2 weeks of age, stress increased plasma corticosterone level. During young adulthood, plasma TNF-α and glucose concentrations increased, whereas plasma insulin and pancreatic HB9 protein levels decreased in Early life stress group. Whereas, Early + young adulthood stress group showed no change in the study parameters, except for plasma corticosterone and insulin concentrations. Overall, early life stress reduced pancreatic HB9 protein expression possibly by elevating plasma corticosterone and TNF-α levels in early life and adulthood, respectively. However, combined with adulthood stress, HB9 protein expression increased to the level of Control. [ABSTRACT FROM AUTHOR]

Early-life stress (ELS) increases the risk of metabolic disorders in later life. The present study investigated the ELS effect on pancreatic pyruvate dehydrogenase (PDH) protein level, α-ketoglutarate dehydrogenase (α-KGDH), and aconitase activities as metabolic enzymes in response to young adulthood stress in male rat offspring. Male Wistar rats were divided into six groups: Control, early life stress (Early STR), young adult foot-shock stress (Y. adult F-SH STR), early + young adult foot-shock stress (Early + Y. adult F-SH STR), young adult psychological stress (Y. adult Psy STR) and early + young adult psychological stress (Early + Y. adult Psy STR). Stress was induced by a communication box at 2 weeks of age and young adulthood for five consecutive days. The blood samples were collected in young adult rats, then pancreases were removed to measure its PDH protein level and aconitase and α-KGDH activities. In ELS animals, applying foot-shock stress in young adulthood increased PDH protein level, decreased α-KGDH and aconitase activities, and increased plasma glucose, insulin, and corticosterone concentrations. However, exposure to young adulthood psychological stress only decreased α-KGDH and aconitase activities. It seems that ELS altered metabolic response to young adulthood stress through changes of Krebs cycle-related enzymes activities, though the type of adulthood stress was determinant. [ABSTRACT FROM AUTHOR]

Introduction: The brain glutamate neurotransmitter system and its NMDA (N-methyl-Daspartate) receptors in the nucleus accumbens play an important role in the incidence of sensitivity and addiction. The present study examined the inhibitory effect of glutamate NMDA receptors in the nucleus accumbens in response to chronic stress. Methods: After the unilateral and bilateral placement of cannula(e) in the nucleus accumbens, one group of the animals received different doses of intra-accumbens memantine (0.1, 0.5 and 1 μg/mouse) 5 minutes before receiving the electric shock stress at their soles (using a Communication Box) and the other group received intraperitoneal memantine (doses of 0.1, 0.5 and 1mg/kg) 30 minutes before receiving the same shock. Chronic stress increased the animals' weight, plasma corticosterone, food and water intake, but reduced their defecation rates and eating latency. Results: The intraperitoneal administration of memantine increased plasma corticosterone, water intake, fecal weight, and eating latency, but had no effect on food intake or weight. The dose and site-dependent intra-accumbens administration of memantine either exacerbated the effects of stress on plasma corticosterone levels, water and food intake, or had no effect on these parameters. Furthermore, the administration of memantine had no effect on animal's weight and inhibited the effects of stress on fecal weight and eating latency. Discussion: The inhibition of glutamate NMDA receptors in the nucleus accumbens can inhibit and/or exacerbate the dose and site-dependent effects of chronic stress, and gender plays a significant role in producing this effect too. [ABSTRACT FROM AUTHOR]

Introduction: In this study, the effect of memantine administration into the nucleus accumbens on the metabolic changes induced by acute stress in female mice was evaluated. Methods: Intra-accumbens unilateral or bilateral canulation was performed. One week after recovery, a group of animals were given memantine (1, 0.5, and 0.1 μg/mouse) five min before stress induction intra-accumbally, and the other group received it (1, 0.5 and 0.1 mg/kg) 30 min before stress intraperitoneally. Food and water intake, weight of fecal material, and the delay time before eating were measured as metabolic parameters after stress induction. Results: Acute stress reduced water and food intake, fecal matter, and the delay time before eating. Intraperitoneal memantine injections augmented the stress effect on water intake, but inhibited its effect on food intake at dose of 0.1 mg/kg and had no impact on defecation. The drug induced anorexia especially at dose of 1 mg/kg. On the other hand, intra-accumbens memantine injections reduced water intake when the drug was injected in the left side. Moreover, memantine injections inhibited or enhanced the effects of stress on water intake, food intake and defecation in a doseand location-dependent manner, and also increased the delay time before eating. Conclusion: Memantine inhibits or enhances the effects of acute stress dose-dependently. In addition, it seems that there is asymmetry in nucleus accumbens response. [ABSTRACT FROM AUTHOR]