Seasonal changes in glucose tolerance and glycogen disposition in a lizard

1963 ◽  
Vol 204 (4) ◽  
pp. 677-680 ◽  
Author(s):  
Anthony Di Maggio ◽  
Herbert C. Dessauer
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Seasonal Changes ◽  
Liver Glycogen ◽  
Early Summer ◽  
Anolis Carolinensis ◽  
Fasting Level ◽  
Glucose Injection ◽  
Different Seasons ◽  
Autumn And Winter

Forty milligrams of glucose in 0.4 ml of water were injected intraperitoneally into fasted adult male lizards, Anolis carolinensis, in different seasons. At intervals of 3 hr to 5 days following injection lizards were sacrificed and their tissues analyzed for carbohydrate. Blood glucose returned to fasting level in less than 36 hr in spring and summer but remained above fasting level for over 2 days during autumn and winter. Generally, 4–6 g of glycogen were deposited per 100 g of liver per day. Greater quantities of glycogen were deposited in liver during autumn than in other seasons. The rate of decrease of liver glycogen was slowest in autumn and winter. Extrahepatic glycogen did not increase after glucose injection in early summer and autumn but rose significantly in winter and spring. The decreased "glucose tolerance" of Anolis and its increased capacity to store glycogen in autumn and winter may be due to a decreased rate of carbohydrate oxidation in these seasons.

Metabolic background for glucose tolerance: mechanism for epinephrine-induced impairment

1975 ◽  
Vol 229 (4) ◽  
pp. 955-961 ◽  
Author(s):  
H Skikama ◽  
M Ui
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Glucose Tolerance ◽  
Glucose Uptake ◽  
Liver Glycogen ◽  
Glucose Load ◽  
Turnover Rates ◽  
Tolerance Mechanism

Turnover rates of blood glucose in rats were calculated from the decay of [14C]glucose. A glucose load suppressed glucose appearance and this was reversed by epinephrine or glucagon. Incorporation of [14C]bicarbonate into liver glycogen and blood glucose demonstrated that these hormones did not alter gluconeogetic rate but, rather the proportion of glucose recovered in the two products. The glucose enhanced by glucagon, probably through increased insulin secretion. In contrast, epinephrine decreased peripheral glucose uptake.

Effect of fast and hexose injection on serum insulin concentrations of sheep

1964 ◽  
Vol 206 (2) ◽  
pp. 419-424 ◽  
Author(s):  
J. M. Boda
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Serum Insulin ◽  
Biologically Active ◽  
Utilization Rate ◽  
Exogenous Glucose ◽  
Glucose Injection ◽  
Tenfold Increase ◽  
Low Glucose ◽  
Blood Glucose Concentrations

Immunoreactive serum insulin concentration in 15 wethers fasted 16–24 hr was 126 ± 12 µU/ml. Exogenous glucose produced a tenfold increase in serum insulin within 15 min; concentrations remained high for 1 hr and then declined. Fructose increased both blood glucose and insulin. The maximum response of the latter was delayed, in comparison with that produced by glucose injection, and coincided with a rise of blood glucose derived from fructose conversion. Galactose produced a moderate and immediate rise in insulin associated with elevated blood glucose concentrations. There was a positive relationship between the amount of insulin secreted and the utilization rate of injected glucose. Thus, insulin released by glucose loading in the sheep is both immunologically and biologically active. Prolonged fasting depressed glucose tolerance and the amount of insulin secreted following glucose injection. Certain characteristics of the sheep, such as reduced glucose tolerance and low glucose oxidation, are not due to a relative lack of circulating insulin or to an inability of hyperglycemia to mobilize insulin stores.

Glucose load diverts hepatic gluconeogenic product from glucose to glycogen in vivo.

1978 ◽  
Vol 235 (4) ◽  
pp. E354
Author(s):  
H Shikama ◽  
M Ui
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Specific Activity ◽  
Hepatic Metabolism ◽  
Liver Glycogen ◽  
Metabolic Changes ◽  
Glucose Load ◽  
Endogenous Insulin ◽  
Fasted Rats

Intravenous or oral administration of concentrated glucose solution into fasted rats simultaneously injected with 14C-bicarbonate resulted in an inhibition of [14C]glucose release into the blood and in an accelerated [14C]glycogen formation associated with glycogen synthetase activation and phosphorylase inactivation in the liver. The specific activity of glycogen was much higher than that of blood glucose after the glucose load, indicating that glycogen originated from gluconeogenesis rather than blood glucose. These metabolic changes induced by the glucose load were not mediated by endogenous insulin because they were observed to the same extent in rats treated with anti-insulin serum. However, they were mostly, if not totally, abolished by adrenalectomy, which suppressed gluconeogenesis and glycogenesis. Glucose tolerance was markedly impaired not only by anti-insulin serum, which inhibits peripheral glucose utilization, but also by adrenalectomy, which affects hepatic metabolism. It is concluded that a glucose load diverts the final product of hepatic gluconeogenesis from blood glucose to liver glycogen; these metabolic changes in the liver are an important determinant of glucose tolerance.

Mentha pulegium Aqueous Extract Exhibits Antidiabetic and Hepatoprotective Effects in Streptozotocin-Induced Diabetic Rats

2019 ◽  
Vol 19 (3) ◽  
pp. 292-301
Author(s):  
Omar Farid ◽  
Naoufel Ali Zeggwagh ◽  
Fadwa EL Ouadi ◽  
Mohamed Eddouks
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Aqueous Extract ◽  
Morphometric Analysis ◽  
Diabetic Rats ◽  
Mentha Pulegium ◽  
Glucose Levels ◽  
Histological Sections ◽  
Blood Glucose Levels ◽  
Liver And Pancreas

Objective: The aim of this work was to evaluate the antihyperglycemic activity of aerial parts aqueous extract (A.P.A.E) of Mentha pulegium (M. pulegium) on blood glucose levels in normal and streptozotocin(STZ)-induced diabetic rat. The glucose tolerance was evaluated in normal rats. Moreover, the histological sections and morphometric analysis at the liver and pancreas have been carried out in this investigation both in normal and STZ-diabetic rats. Methods: The effect of A.P.A.E of M. pulegium (20 mg/kg) on blood glucose levels was investigated in normal and diabetic rats (n=6). Histopathological changes in liver and pancreas were examined under phase contrast microscope and a preliminary screening for various bioactive constituents was realized according to standard methods. Key Findings: Both single and repeated oral administration of A.P.A.E (20 mg/kg) caused a significant reduction in blood glucose levels in STZ-diabetic rats (p<0.0001). The morphometric analysis and histological sections realized in pancreas and liver have showed the beneficial effect of the A.P.A.E in cellular population. According to oral glucose tolerance test (OGTT), the aqueous extract has revealed an improvement of glucose tolerance in normal rat. Furthermore, the preliminary phytochemical screening of A.P.A.E of M. pulegium has demonstrated the presence of various metabolite compounds including polyphenols, flavonoids, terpenoids tannins, cyanidins, sesquiterpenes, and glycosides. Conclusion: We conclude that the A.P.A.E of M. pulegium (20 mg/kg) exhibits a potent antihyperglycemic activity in STZ diabetic rats.

Carbohydrate metabolism of mice exposed to simulated changes in gravity

1964 ◽  
Vol 207 (2) ◽  
pp. 411-414 ◽  
Author(s):  
Jiro Oyama ◽  
William T. Platt
Keyword(s):  
Blood Glucose ◽  
Carbohydrate Metabolism ◽  
Exposure Time ◽  
Liver Glycogen ◽  
Critical Function ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Significant Difference ◽  
Glycogen Deposition ◽  
Adrenal Corticosterone

Unrestrained mice were centrifuged for varying periods ranging from 0.5 to 10 hr at 2.5, 5, and 10 x gravity. Liver glycogen and blood glucose levels increased significantly depending on the g load and exposure time. Adrenalectomy completely abolished the glycogen deposition response. The glycogen response was a critical function of the age of mice; unweaned mice did not respond. Blood corticosterone increased significantly prior to the deposition of glycogen. Centrifuged fed mice deposited three times the amount of glycogen of fasted mice. There was no significant difference in the amount of glycogen deposited in centrifuged mice previously starved for 1, 2, or 3 days. It is concluded that the increased glycogen deposited following centrifugation is effected by an increased elaboration of adrenal corticosterone.

Effects of Different Frequencies of Electroacupuncture on Blood Glucose Tolerance Patients

2014 ◽  
Vol 20 (5) ◽  
pp. A44-A44
Author(s):  
Hong Meng ◽  
Jindong Hao ◽  
Hongcai Wang ◽  
Jiayong Zhao ◽  
Chenlai Zhao ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance

scholarly journals Deletion of CaMKK2 from the Liver Lowers Blood Glucose and Improves Whole-Body Glucose Tolerance in the Mouse

2012 ◽  
Vol 26 (2) ◽  
pp. 281-291 ◽  
Author(s):  
Kristin A. Anderson ◽  
Fumin Lin ◽  
Thomas J. Ribar ◽  
Robert D. Stevens ◽  
Michael J. Muehlbauer ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Protein Kinase ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
De Novo Lipogenesis ◽  
Whole Body ◽  
Peroxisome Proliferator ◽  
Dependent Protein Kinase ◽  
Peroxisome Proliferator Activated Receptor ◽  
Dependent Protein

Abstract Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) is a member of the Ca2+/CaM-dependent protein kinase family that is expressed abundantly in brain. Previous work has revealed that CaMKK2 knockout (CaMKK2 KO) mice eat less due to a central nervous system -signaling defect and are protected from diet-induced obesity, glucose intolerance, and insulin resistance. However, here we show that pair feeding of wild-type mice to match food consumption of CAMKK2 mice slows weight gain but fails to protect from diet-induced glucose intolerance, suggesting that other alterations in CaMKK2 KO mice are responsible for their improved glucose metabolism. CaMKK2 is shown to be expressed in liver and acute, specific reduction of the kinase in the liver of high-fat diet-fed CaMKK2floxed mice results in lowered blood glucose and improved glucose tolerance. Primary hepatocytes isolated from CaMKK2 KO mice produce less glucose and have decreased mRNA encoding peroxisome proliferator-activated receptor γ coactivator 1-α and the gluconeogenic enzymes glucose-6-phosphatase and phosphoenolpyruvate carboxykinase, and these mRNA fail to respond specifically to the stimulatory effect of catecholamine in a cell-autonomous manner. The mechanism responsible for suppressed gene induction in CaMKK2 KO hepatocytes may involve diminished phosphorylation of histone deacetylase 5, an event necessary in some contexts for derepression of the peroxisome proliferator-activated receptor γ coactivator 1-α promoter. Hepatocytes from CaMKK2 KO mice also show increased rates of de novo lipogenesis and fat oxidation. The changes in fat metabolism observed correlate with steatotic liver and altered acyl carnitine metabolomic profiles in CaMKK2 KO mice. Collectively, these results are consistent with suppressed catecholamine-induced induction of gluconeogenic gene expression in CaMKK2 KO mice that leads to improved whole-body glucose homeostasis despite the presence of increased hepatic fat content.

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