Hypothalamic noradrenergic and sympathoadrenal control of glycemia after stress

1989 ◽  
Vol 256 (2) ◽  
pp. E231-E235
Author(s):  
G. A. Smythe ◽  
W. S. Pascoe ◽  
L. H. Storlien
Keyword(s):  
Insulin Release ◽  
Acute Stress ◽  
Serum Insulin ◽  
Elevated Serum ◽  
Serum Glucose ◽  
Neural Pathways ◽  
Swim Stress ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Positive Correlations

Central noradrenergic pathways play a significant role in mediating blood glucose levels after neuroglycopenia. To further investigate hypothalamic noradrenergic neuronal activity (NNA) and sympathoadrenal influences in glucoregulation, we studied the effects of acute stress on glycemia and insulin release in normal and adrenalectomized (ADRX) rats. Within 5 min of exposure of rats to ether or cold-swim stress, significant positive correlations were evident between hypothalamic NNA and serum glucose levels (r = 0.70, P less than 0.001; at 15 min r = 0.78, P less than 0.0001). Five minutes after stress in the intact rat, insulin release was inhibited and serum insulin levels inversely correlated to hypothalamic NNA (r = 0.45, P less than 0.05). This relationship between insulin and NNA was no longer present 15 min after stress, but the levels of insulin remained inappropriately low with respect to the elevated serum glucose levels (approximately 30% above basal). Blockade of sympathetic noradrenergic pathways by treatment of intact rats with guanethidine prevented the rise in glucose after cold-swim stress but did not prevent the inhibition of insulin release. Fifteen minutes after exposure of ADRX rats to cold-swim stress their hypothalamic NNA and serum glucose levels were similar to intact animals. However, in contrast to their intact counterparts, serum insulin levels were significantly elevated (P less than 0.01). These data are consistent with central noradrenergic neural pathways directly mediating hepatic glucose release and indirectly inhibiting pancreatic insulin release via activation of adrenal medullary catecholamines.

scholarly journals Effect of in ovo ghrelin administration on subsequent serum insulin and glucose levels in newly-hatched chicks

2011 ◽  
Vol 56 (No. 8) ◽  
pp. 377-380 ◽  
Author(s):  
A. Lotfi ◽  
H. Aghdam-Shahryar ◽  
J. Ghiasi-Ghalehkandi ◽  
H. Kaiya ◽  
N. Maheri-Sis
Keyword(s):  
Animal Species ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Avian Embryo ◽  
Regulatory Peptide ◽  
In Ovo ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Hatching Time ◽  
Embryonic Life

Ghrelin is a regulatory peptide in glucose homeostasis in animal species. Its effect in the avian embryo is unclear. The aim of this study was to investigate the effects of in ovo ghrelin administration on serum glucose and insulin levels of hatched chicks. A total of 250 fertilized eggs were divided into 5 groups; group T1 as control (without injection), group T2 (in ovo injected with 50 ng/egg ghrelin on day 5), group T3 (in ovo injected with 100 ng/egg ghrelin on day 5), group T4 (in ovo injected with 50 ng/egg ghrelin on day 10) and group T5 (in ovo injected with 100 ng/egg ghrelin on day 10). After hatching, serum insulin and glucose concentrations were determined. Group T4 and T5 showed significantly higher serum insulin levels (0.43 and 0.60 ng/ml, respectively) compared with T1, T2 and T3 (0.09, 0.10, and 0.23 ng/ml, respectively) in hatched chicks. Glucose concentrations have not been affected by in ovo administered ghrelin in all injected groups. It seems that embryonic β-cells were stimulated to secrete a considerable level of insulin in response to in ovo ghrelin in the late embryonic life. The observed stability of glucose rate suggests the incidence of insulin resistance at hatching time or in newly hatched chicks from in ovo ghrelin administered eggs on day 10.

Comparative evaluation of atenolol and metoprolol on cardiovascular complications associated with streptozotocin-induced diabetic rats

2007 ◽  
Vol 85 (8) ◽  
pp. 831-836 ◽  
Author(s):  
Shraddha V. Bhadada ◽  
Ramesh K. Goyal
Keyword(s):  
Heart Rate ◽  
Serum Insulin ◽  
Cardiovascular Complications ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Cardiac Tissues ◽  
Insulin Levels ◽  
Beneficial Effects ◽  
Glucose Levels

Recently, various clinical studies have indicated that lipophilic β-blockers reduce the coronary mortality in diabetic patients; however, systematic studies have not been reported. The objective of the present investigation was to compare the effects of chronic treatment with metoprolol and atenolol on cardiovascular complications in streptozotocin (STZ)-induced diabetic rats. Injection of STZ produced hyperglycemia, hypoinsulinemia, hyperlipidemia, increased blood pressure, cardiac hypertrophy, reduction in heart rate, and structural alterations in cardiac tissues. Metoprolol and atenolol effectively prevented the development of hypertension in diabetic rats. Metoprolol treatment produced a slight but significant reduction in serum glucose levels with elevation in serum insulin levels, while atenolol produced a slight increase in glucose levels but no effect on insulin levels. Moreover, neither metoprolol nor atenolol treatment reduced the elevated cholesterol levels in diabetic rats. Metoprolol treatment significantly prevented STZ-induced increase in triglyceride levels, but atenolol failed to produce this effect. Metoprolol exhibited a minimal improvement in STZ-induced bradycardia, whereas atenolol produced a further reduction in heart rate. Histological examination showed metoprolol treatment also prevented STZ-induced hypertrophy and some of the alterations in cardiomyocytes. In conclusion, our data suggest that metoprolol has some beneficial effects over atenolol with respect to cardiovascular complications associated with diabetes mellitus.

Hepatoprotective effects of selenium during diabetes in rats

2015 ◽  
Vol 35 (2) ◽  
pp. 114-123 ◽  
Author(s):  
C Zou ◽  
Q Qiu ◽  
H Chen ◽  
L Dou ◽  
J Liang
Keyword(s):  
Enzyme Activities ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Total Glutathione ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Selenium Treatment ◽  
Male Wistar Rats

The present study investigated the hepatoprotective role of selenium during alloxan-induced diabetes in rats. Male Wistar rats were divided into four groups, namely, normal control, selenium treated, diabetic, and selenium-treated diabetic. Diabetes was induced in the animals by injecting alloxan intraperitoneally at a dose rate of 150 mg/kg body weight. Selenium in the form of sodium selenite was supplemented to rats at a dose level of 1 ppm in drinking water, ad libitum for two time durations of 2 and 4 weeks. The effects of different treatments were studied on various parameters in rat liver, which included serum glucose levels, serum insulin levels, alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lipid peroxidation (LPO), glutathione reduced (GSH), oxidized glutathione (GSSG), total glutathione (TG), superoxide dismutase (SOD), catalase (CAT), glutathione reductase, glutathione peroxidase, metallothionein (MT), and histoarchitecture. A significant increase in the serum glucose levels, LPO levels, and in enzyme activities of ALP, ALT, and AST was observed in diabetic rats which, however, got decreased significantly upon supplementation with selenium. On the contrary, decreased enzyme activities of GSSG, SOD, and CAT and depressed levels of GSH as well as serum insulin levels were observed in diabetic rats which got improved following selenium supplementation. Interestingly, MT levels were increased both in diabetic and selenium-treated diabetic rats. Further, marked alterations in histoarchitecture were seen in diabetic rats with the prominent features being congestion in sinusoids, lipid accumulation, and centrilobular hepatocyte degeneration. However, selenium treatment to diabetic rats showed overall improvement in the hepatic histoarchitecture.

scholarly journals Endothelial dysfunction precedes hypertension in diet-induced insulin resistance

1998 ◽  
Vol 275 (3) ◽  
pp. R788-R792 ◽  
Author(s):  
Prasad V. G. Katakam ◽  
Michael R. Ujhelyi ◽  
Margarethe E. Hoenig ◽  
Allison Winecoff Miller
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Mesenteric Arteries ◽  
Control Group ◽  
Sprague Dawley ◽  
Insulin Resistant ◽  
Glucose Levels

The insulin-resistant (IR) syndrome may be an impetus for the development of hypertension (HTN). Unfortunately, the mechanism by which this could occur is unclear. Our laboratory and others have described impaired endothelium-mediated relaxation in IR, mildly hypertensive rats. The purpose of the current study is to determine if HTN is most likely a cause or result of impaired endothelial function. Sprague-Dawley rats were randomized to receive a fructose-rich diet for 3, 7, 10, 14, 18, or 28 days or were placed in a control group. The control group received rat chow. After diet treatment, animals were instrumented with arterial cannulas, and while awake and unrestrained, their blood pressure (BP) was measured. Subsequently, endothelium-mediated relaxation to acetylcholine was determined (in vitro) by measuring intraluminal diameter of phenylephrine-preconstricted mesenteric arteries (∼250 μM). Serum insulin levels were significantly elevated in all groups receiving fructose feeding compared with control, whereas there were no differences in serum glucose levels between groups. Impairment of endothelium-mediated relaxation starts by day 14 [mean percent maximal relaxation (Emax): 69 ± 10% of baseline] and becomes significant by day 18 (Emax: 52 ± 11% of baseline; P < 0.01). However, the mean BP (mmHg) does not become significantly elevated until day 28 [BP: 132 ± 1 ( day 28) vs. 116 ± 3 (control); P < 0.05]. These findings demonstrate that both IR and endothelial dysfunction occur before HTN in this model and suggest that endothelial dysfunction may be a mechanism linking insulin resistance and essential HTN.

scholarly journals Dexamethasone Administration in Mice Leads to Less Body Weight Gain over Time, Lower Serum Glucose, and Higher Insulin Levels Independently of NRF2

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 4
Author(s):  
Fotini Filippopoulou ◽  
George I. Habeos ◽  
Vagelis Rinotas ◽  
Antonia Sophocleous ◽  
Gerasimos P. Sykiotis ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Body Weight Gain ◽  
Serum Glucose ◽  
Dexamethasone Treatment ◽  
Insulin Levels ◽  
Glucose Levels ◽  
High Insulin

Glucocorticoids are used widely on a long-term basis in autoimmune and inflammatory diseases. Their adverse effects include the development of hyperglycemia and osteoporosis, whose molecular mechanisms have been only partially studied in preclinical models. Both these glucocorticoid-induced pathologies have been shown to be mediated at least in part by oxidative stress. The transcription factor nuclear erythroid factor 2-like 2 (NRF2) is a central regulator of antioxidant and cytoprotective responses. Thus, we hypothesized that NRF2 may play a role in glucocorticoid-induced metabolic disease and osteoporosis. To this end, WT and Nrf2 knockout (Nrf2KO) mice of both genders were treated with 2 mg/kg dexamethasone or vehicle 3 times per week for 13 weeks. Dexamethasone treatment led to less weight gain during the treatment period without affecting food consumption, as well as to lower glucose levels and high insulin levels compared to vehicle-treated mice. Dexamethasone also reduced cortical bone volume and density. All these effects of dexamethasone were similar between male and female mice, as well as between WT and Nrf2KO mice. Hepatic NRF2 signaling and gluconeogenic gene expression were not affected by dexamethasone. A 2-day dexamethasone treatment was also sufficient to increase insulin levels without affecting body weight and glucose levels. Hence, dexamethasone induces hyperinsulinemia, which potentially leads to decreased glucose levels, as well as osteoporosis, both independently of NRF2.

scholarly journals Effect of metformin on the expression of SNAER proteins in the skeletal muscle of rats with type 2 diabetes

2021 ◽  
pp. 270-278
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Body Weight ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Snare Complex ◽  
Snare Proteins ◽  
Glucose Levels ◽  
Male Wistar Rats

Background and Aims: SNARE proteins are composed of a combination of SNAP-23, Stx-4, and VAMP-2 isoforms that are significantly expressed in skeletal muscle. These proteins control the transport of GLUT4 to the cell membranes. The modifications in the expression of SNARE proteins can cause Type 2 diabetes. The present study aimed to assess the effect of metformin on the expression of these proteins in rats. Materials and Methods: For the purpose of the study, 40 male Wistar rats were randomly selected. Streptozotocin and Nicotinamide were used for the induction of type 2 diabetes. The animals were assigned to five groups (n=8), including healthy and diabetic groups as control, as well as three experimental groups which were treated with different doses of metformin (100, 150, and 200 mg/kg body weight) for 30 days. The quantitative reverse transcription PCR (RT-qPCR) method was applied to evaluate the expression of SNARE complex proteins.. Results: Based on the results, metformin (100, 150, and 200 mg/kg body weight) decreased serum glucose levels and increased serum insulin levels. This difference in dose of 200 mg/kg body weight was statistically significant (P<0.05). Moreover, all three doses of metformin increased the expression of SNAP- 23, syntaxin-4, and VAMP-2 proteins in skeletal muscle tissue. Metformin at a dose of 200 mg/kg body weight demonstrated the most significant effects (P<0.05). Conclusion: As evidenced by the results of the current study, another anti-diabetic mechanism of metformin is to increase the expression of SNARE proteins, which effectively improves insulin resistance and lowers blood glucose.

scholarly journals Aerobic exercise improves LPS-induced sepsis via regulating the Warburg effect in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xishuai Wang ◽  
Zhiqing Wang ◽  
Donghui Tang
Keyword(s):  
Blood Glucose ◽  
Mrna Expression ◽  
Serum Insulin ◽  
Pulmonary Inflammation ◽  
Aortic Injury ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Blood Glucose Levels

AbstractWe investigated the impact of aerobic exercise (AE) on multiple organ dysfunction syndrome (MODS), aortic injury, pathoglycemia, and death during sepsis. ICR mice were randomized into four groups: Control (Con), Lipopolysaccharide (LPS), Exercise (Ex), and Exercise + LPS (Ex + LPS) groups. Mice were trained with low-intensity for 4 weeks. LPS and Ex + LPS mice received 5 mg/kg LPS intraperitoneally for induction of sepsis. Histopathological micrographs showed the organ morphology and damage. This study examined the effects of AE on LPS-induced changes in systemic inflammation, pulmonary inflammation, lung permeability, and bronchoalveolar lavage fluid (BALF) cell count, oxidative stress-related indicators in the lung, blood glucose levels, plasma lactate levels, serum insulin levels, plasma high-mobility group box 1 (HMGB1) levels, glucose transporter 1 (Glut1) and HMGB1, silent information regulator 1 (Sirt-1), and nuclear factor erythroid 2-related factor 2 (Nrf-2) mRNA expression levels in lung tissue. AE improved sepsis-associated multiple organ dysfunction syndrome (MODS), aortic injury, hypoglycemia, and death. AE prominently decreased pulmonary inflammation, pulmonary edema, and modulated redox balance during sepsis. AE prominently decreased neutrophil content in organ. AE prominently downregulated CXCL-1, CXCL-8, IL-6, TNF-α, Glu1, and HMGB1 mRNA expression but activated IL-1RN, IL-10, Sirt-1, and Nrf-2 mRNA expression in the lung during sepsis. AE decreased the serum levels of lactate and HMGB1 but increased blood glucose levels and serum insulin levels during sepsis. A 4-week AE improves sepsis-associated MODS, aortic injury, pathoglycemia, and death. AE impairs LPS-induced lactate and HMGB1 release partly because AE increases serum insulin levels and decreases the levels of Glut1. AE is a novel therapeutic strategy for sepsis targeting aerobic glycolysis.

scholarly journals A case of glucose-sensitive insulinoma accompanied by slightly elevated serum insulin levels and persisting convulsions after the surgically removed neuroendocrine tumor

2013 ◽  
Vol 154 (2) ◽  
pp. 69-73
Author(s):  
Zsuzsanna Soós ◽  
Anna Czégeni ◽  
Ferenc Salamon ◽  
Mónika Salamon ◽  
István Kenessey ◽  
...  
Keyword(s):  
Neuroendocrine Tumor ◽  
Pancreatic Beta Cells ◽  
Serum Insulin ◽  
Correct Diagnosis ◽  
Elevated Serum ◽  
Pancreatic Neuroendocrine Tumor ◽  
Residual Tumor ◽  
Surgical Removal ◽  
Von Hippel Lindau ◽  
Insulin Levels

Insul(in)oma is a usually solitary or, in some cases, multifocal tumor of pancreatic beta cells. It may be a component of multiple endocrine neoplasia type 1. or von Hippel-Lindau syndrome. In typical forms the diagnosis – based on the Whipple triad – is simple, however, it may be difficult to recognize in cases with near normal or only slightly elevated serum insulin levels, as well as in patients with known convulsive episodes. With the case presentation of an 81-year-old woman the authors draw attention to the pitfalls of the correct diagnosis. A special feature of the presented case is that convulsions persisted after surgical removal of the pancreatic neuroendocrine tumor verified with functional and imaging methods. Recurrant or residual tumor was not found, and morphological damage of the brain was absent. In the background of the continuing convulsions cerebrovascular alterations as well as the cytotoxic effect of the hypoglycemia-induced excessive glutamate production can be postulated. Orv. Hetil., 2013, 154, 69–73.

Changes in Levels of Serum Insulin, C-Peptide and Glucose after Electroacupuncture and Diet Therapy in Obese Women

2006 ◽  
Vol 34 (03) ◽  
pp. 367-376 ◽  
Author(s):  
Mehmet Tuğrul Cabıoğlu ◽  
Neyhan Ergene
Keyword(s):  
Weight Loss ◽  
Serum Insulin ◽  
Diet Therapy ◽  
Serum Glucose ◽  
The Body ◽  
Obese Women ◽  
Diet Restriction ◽  
C Peptide ◽  
Glucose Levels ◽  
Restriction Group

Our purpose was to investigate the effects of electroacupuncture (EA) therapy on body weight and on levels of serum insulin, c-peptide and glucose in obese women. 52 healthy women were included in this study and were allocated into three groups: 1) Placebo EA group ( n = 15; mean age = 41.8 ± 4.6 and mean body mass index { BMI } = 33.2 ± 3.5); 2) EA group ( n = 20; mean age = 42.1 ± 4.4 and BMI = 35.9 ± 3.6) and 3) Diet restriction group ( n = 20; mean age = 42.9 ± 4.3 and BMI = 34.7 ± 2.7). EA was applied to the ear points Hunger and Shen Men on alternating days and to the body points LI 4, LI 11, St 36 and St 44 once a day for 30 minutes over 20 days. Diet restriction that entailed a 1450 kilocalorie (kcal) diet program was applied to the three groups for 20 days. An increase in weight loss was observed when weight loss in the EA group (p < 0.000) was compared to that in the diet restricted and placebo EA groups using the Tukey HSD test. There were increases in the serum insulin (p < 0.001) and c-peptide levels (p < 0.000) in the women treated with EA compared to those in the women treated with the placebo EA and diet restriction groups. A decrease was observed in the glucose levels (p < 0.01)in both the EA and diet restriction groups compared to those in the placebo EA group. Our results suggest that EA therapy is an effective method in treating obesity. EA therapy also helps serum glucose levels to decrease through the increase of serum insulin and c-peptide levels.

Glucose can reverse the effects of acute fasting on mouse ovulation and oocyte maturation

2008 ◽  
Vol 20 (6) ◽  
pp. 703 ◽  
Author(s):  
Jun Yan ◽  
Bo Zhou ◽  
Jie Yang ◽  
Ping Tai ◽  
Xiufen Chen ◽  
...  
Keyword(s):  
Food Deprivation ◽  
Oocyte Maturation ◽  
Elevated Serum ◽  
Glucose Consumption ◽  
Serum Glucose ◽  
Oocyte Development ◽  
Serum Progesterone ◽  
Glucose Levels ◽  
Glucose Feeding

Food deprivation suppresses ovulation. Although nutritional elements are responsible for this suppression, it is not clear whether energy metabolism has any effect on oocyte development under these circumstances. The aim of the present study was to determine which nutritional element is responsible for the effect of acute fasting on mouse ovulation and how oocyte development is affected. The results demonstrate that 64 h food deprivation blocks mouse ovulation. This was reversed by glucose feeding, oil feeding or short-term feeding, all of which elevated serum glucose levels. Furthermore, 48 h food deprivation inhibited follicle-stimulating hormone-induced oocyte maturation in vitro. However, 48 h glucose feeding increased serum glucose levels and restored oocyte maturation. Food deprivation increased serum progesterone levels and decreased serum oestradiol levels. Food deprivation also impaired follicle development, caused the death of oocytes and attenuated glucose consumption by cumulus–oocyte complexes. Taken together, the results indicate that: (1) the suppression of ovulation by acute fasting may be due to the control of oocyte development; and (2) maintaining serum glucose concentrations at a certain level is important for normal ovulation.

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