Glucose Homeostasis In Rats Research Articles

Erythrocytes and glucose homeostasis in rats

Erythrocytes and glucose homeostasis in rats

Erythrocytes and glucose homeostasis in rats.

The capacity of erythrocytes to modify their glycogen stores to compensate for changes in glucose concentration in plasma was studied. Experiments in vitro and in vivo demonstrated that erythrocytes absorbed and incorporated glucose into their glycogen stores when glucose concentration in the medium was high and liberated it when the concentration was low. Epinephrine administration inhibited glucose absorption by erythrocytes, and in its presence, erythrocytes liberated glucose from their glycogen stores, being unable to compensate for this rise in glucose concentration in plasma. Similar results were obtained when endogenous secretion of epinephrine was enhanced by carotid sinus-chemoreceptor stimulation. Insulin had no effect on the capacity of erythrocytes to absorb glucose. These data suggest a role for erythrocytes in the transport of glucose to different regions in the organism's circulation and in the regulation of glucose concentration in plasma.

Long term improvement of glucose homeostasis by vanadate treatment in diabetic rats.

The trace element vanadium (V) exerts insulin-like effects in vitro. The present study examined its effects on glucose homeostasis in rats made diabetic by streptozotocin. Na3VO4 (0.2 or 0.5 mg/ml) was administered ad libitum in drinking water. Fed plasma glucose levels (approximately 26 mmol/liter) fell by 30% and 56% after 5 days of treatment with the low (VO.2) and high (VO.5) concentrations of vanadate, respectively. This decrease was not due to a rise in peripheral insulin levels and persisted for more than 2 months. Daily glucosuria was decreased by 60% and 85% in VO.2 and VO.5 rats, respectively. Tolerance of the rats to oral or iv glucose was also considerably improved by vanadate; integrated glucose responses were about 55% and 75% lower in VO.2 and VO.5 rats than in controls, and the differences were not due to restoration of insulin release. Compared to nondiabetic rats, pancreatic insulin reserves amounted to 1% in untreated rats, 3% in VO.2 rats, and 6% in VO.5 rats after 9 weeks of treatment. Liver, but not muscle, glycogen was increased by vanadate. Despite improvement of their diabetic state, vanadate-treated rats did not gain more weight than untreated rats. Their food intake (corrected for urinary glucose losses) was decreased by about 25%. No signs of altered kidney or liver function were observed in rats receiving vanadate. In conclusion, vanadate markedly improves glucose homeostasis in streptozotocin-diabetic rats by an insulin-like mechanism, but does not reproduce the anabolic effects of the hormone.

Protein-energy malnutrition in pregnant rats improves the adaptation of the endocrine pancreas in malnourished offspring and induces insulin resistance after rehabilitation.

1. In developing countries, malnutrition begins during pregnancy and lactation. Glucose intolerance is a problem of importance during protein-energy malnutrition (PEM). We therefore studied glucose homeostasis in rats weaned from undernourished mothers. 2. On weaning, 156 male Wistar rats, born from deprived mothers (75 g casein/kg diet), were fed ad lib on either a balanced diet (180 g casein/kg; group DR), or a protein-deficient diet (50 g casein/kg; group DD). At seven time intervals (weeks 0, 1, 3, 5, 8, 16 and 23) twelve rats were weighed, fasted overnight and then decapitated. Blood glucose, plasma insulin (IRI) and glucagon (IRG) levels and pancreatic insulin and glucagon contents were determined. 3. In DR and DD rats blood glucose, which was normal at weaning, dropped in the 1st week and then increased slowly. DR rats were hyperglycaemic from week 16. IRI continually increased during the experiment from near-normal values to hyperinsulinic levels in DR rats; in group DD, it remained stable until week 8 before increasing. IRG, which was very low at weaning, increased to normal levels in the 1st week in group DR; in group DD, it fell slightly during the study. Pancreatic hormone contents were much higher than after normal pregnancy and lactation. 4. We compared these results with those of a previous study with rats born from normal mothers: at weaning in the second experiment the rats were already well adapted to malnutrition. The plasma ratio IRI:IRG in DD rats showed two phases of adaptation: weeks 0-5 when glucose homeostasis did not change and weeks 5-23 when it became increasingly normal. At the end of the experiment DR rats still had a lower body-weight than normal rats but were insulin-resistant.

Glucose homeostasis in rats treated acutely and chronically with quinine

Glucose homeostasis in normal rats was studied after chronic or acute administration of quinine. Male rats received a daily dose of 10–30 mg/kg of quinine in the drinking water for 20 weeks. The high dose caused a slight decrease in food intake and weight gain. Though basal plasma insulin levels were increased in treated rats, their plasma glucose levels were only slightly and not consistently decreased. After oral or intravenous administration of glucose, the plasma insulin levels were higher and the disappearance rate of glucose was greater in rats receiving quinine than in the controls. The insulin content of the pancreas was not affected by quinine treatment. Intraperitoneal injection of a high dose of quinine (30 mg/kg) transiently increased plasma glucose and insulin levels. The insulin response was increased during a subsequent administration of glucose but the glucose levels were not modified. This study shows that chronic administration of quinine increases plasma insulin levels, accelerates disposal of oral or intravenous glucose but does not cause hypoglycaemia in normal rats.

The roles of glucagon, insulin and glucocorticoid hormones in the effects of sub-lethal doses of endotoxin on glucose homeostasis in rats

(1) The effects of sub-lethal doses of endotoxin on plasma glucose, glucagon, insulin, glucocorticoids and non-esterified fatty acids (NEFA) were determined in rats. (2) Endotoxin did not change the plasma concentration of glucocorticoids, but blocked the effects of elevated glucocorticoid hormone concentrations on both plasma glucose and hepatic tryptophan dioxygenase activity. (3) Endotoxin increased the plasma concentrations of glucose, glucagon and insulin in rats with basal glucocorticoid concentrations, and changed the observed relationships between glucose, glucagon and insulin in a manner consistent with an increased sensitivity of glucagon secretion to lowered glucose concentrations. (4) At the highest dose of endotoxin used, 20 mg/kg over 6hr, a substantial decrease (>7-fold) in the insulin/glucagon ratio provides evidence for changes in basal (as opposed to hormone-stimulated) glucose production and/or utilisation in vivo.

Blood glucose homeostasis in rats with a deficiency of liver phosphorylase kinase

The glycogen storage disorder (gsd/gsd) rat has little or no phosphorylase kinase activity in the liver and is unable to break down liver glycogen on fasting. Nevertheless, gsd/gsd rats do not become hypoglycaemic on fasting. Gsd/gsd rats showed a decreased rate of glucose turnover measured with [6-3H]glucose. Perfused livers from gsd/gsd rats showed decreased rates of gluconeogenesis from lactate and alanine when the results were expressed per gram of liver, but the total glucose produced per liver was normal. Measurement of gluconeogenesis in vivo using [14C]-bicarbonate showed that gsd/gsd rats had a decreased rate of glucose production from substrates that enter the gluconeogenic pathway before pyruvate. We conclude that gsd/gsd rats have adapted to unavailability of liver glycogen by decreasing peripheral uptake of glucose and not by increasing gluconeogenesis.

Renal net glucose release in vivo and its contribution to blood glucose in rats.

This study describes the contribution of de novo glucose synthesis by the kidney to blood glucose homeostasis in rats. The net glucose release by the kidney in vivo was measured by an isotope-dilution method, which calculated the extent of dilution of injected [(14)C]glucose by glucose newly synthesized in the kidney. The extent of dilution was determined from the difference between the decrease of the actual blood glucose concentration and that of the radioactivity of [(14)C]glucose, after injecting [(14)C]glucose into functionally hepatectomized rats. The results indicate that the net glucose release by the kidney in vivo in normal fed rats was 0.75+/-0.13 mg/dl per min, and that its contribution to blood glucose was 25.9+/-5.0%. When unilateral nephrectomy was performed, under the same conditions, renal net glucose release was one-half of that in rats with two intact kidneys, which indicates the quantitative accuracy of the isotope-dilution method employed in this study. In rats starved for 24 h, the renal net glucose release increased to 0.99+/-0.08 mg/dl per min. Diabetic rats showed a remarkably higher renal net glucose of 2.28+/-0.33 mg/dl per min, which was 360% of the normal level. Treatment of diabetic rats with insulin, restored the renal net glucose release to the normal level. In acidotic rats, renal net glucose release was as great as 1.03+/-0.15 mg/dl per min, which suggests that the acid-base balance participates in control of renal glucose output. Measurements every 6 h throughout the day showed that glucose was supplied from the kidney at a constant rate without any circadian rhythm. These data suggest that renal gluconeogenesis is of physiological importance in the maintenance of homeostasis of blood glucose.

Fasting glucose homeostasis in rats after chronic exposure to hypoxia.

ARTICLESFasting glucose homeostasis in rats after chronic exposure to hypoxiaMB Davidson, and VS AokiMB Davidson, and VS AokiPublished Online:01 Aug 1970https://doi.org/10.1152/ajplegacy.1970.219.2.378MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByFeatures of the Course of Non-alcoholic Fatty Liver Disease in Experimental Animals at High Altitudes19 November 2021 | Open Access Macedonian Journal of Medical Sciences, Vol. 9, No. AMetabolic effects of intermittent hypoxia in mice: steady versus high-frequency applied hypoxia daily during the rest periodAlba Carreras, Foaz Kayali, Jing Zhang, Camila Hirotsu, Yang Wang, and David Gozal1 October 2012 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 303, No. 7Experimental and Transgenic Models of Pulmonary Hypertension1 April 2011Emerging role of adipose tissue hypoxia in obesity and insulin resistance9 December 2008 | International Journal of Obesity, Vol. 33, No. 1Hypoxia is a potential risk factor for chronic inflammation and adiponectin reduction in adipose tissue of ob/ob and dietary obese miceJianping Ye, Zhanguo Gao, Jun Yin, and Qing He1 October 2007 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 293, No. 4Effects of Hypoxia on Glucose, Insulin, Glucagon, and Modulation by Corticotropin-Releasing Factor Receptor Type 1 in the RatEndocrinology, Vol. 148, No. 7Sleep-Disordered Breathing and Metabolic Effects: Evidence from Animal ModelsSleep Medicine Clinics, Vol. 2, No. 2Troubles respiratoires au cours du sommeil, obésité et diabèteMédecine du Sommeil, Vol. 1, No. 1Intermittent Hypoxia Increases Insulin Resistance in Genetically Obese Mice1 October 2003 | The Journal of Physiology, Vol. 552, No. 1Sleep-disordered breathing, glucose intolerance, and insulin resistanceRespiratory Physiology & Neurobiology, Vol. 136, No. 2-3Effect of a carbohydrate supplement on feeding behaviour and exercise in rats exposed to hypobaric hypoxiaAppetite, Vol. 39, No. 2Depressed gluconeogenesis and ureogenesis in isolated hepatocytes after intermittent hypoxia in ratsInternational Journal of Biochemistry, Vol. 22, No. 11Metabolic and Endocrine Changes at AltitudeHepatic effects of glucose and insulin independent of cyclic nucleotide changesActa Diabetologica Latina, Vol. 18, No. 4Stress hyperglycemia and the adrenergic regulation of pancreatic hormones in hypoxiaMetabolism, Vol. 29, No. 11Primary insulin antagonism of glucose transport in muscle from the older-obese ratMetabolism, Vol. 27, No. 12Effect of adaptation to high altitude on components of blood and urine of lowlanders compared with high altitude nativesInternational Journal of Biometeorology, Vol. 18, No. 4 More from this issue > Volume 219Issue 2August 1970Pages 378-383 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.219.2.378PubMed5448067History Published online 1 August 1970 Published in print 1 August 1970 Metrics