scholarly journals Ethanol and glycogen synthesis in cardiothoracic and skeletal muscles following glucose re-feeding after starvation in the rat

1992 ◽  
Vol 288 (2) ◽  
pp. 445-450 ◽  
Author(s):  
D Xu ◽  
R Thambirajah ◽  
T N Palmer
Keyword(s):  
Blood Glucose ◽  
Skeletal Muscles ◽  
Glycogen Synthesis ◽  
Ethanol Administration ◽  
Ethanol Treatment ◽  
Glycaemic Response ◽  
Glucose Administration ◽  
Glycogen Deposition ◽  
Dose Dependent ◽  
Glucose Availability

The pattern of glycogen deposition in individual cardiothoracic and skeletal muscles in response to oral and intraperitoneal glucose administration was examined in 40 h-starved rats. Rates of glycogen synthesis were consistently higher in oxidative muscles than in non-oxidative muscles. Intragastric ethanol administration was associated with an impaired glycaemic response and the almost total abolition of glycogen deposition in oxidative muscles in response to oral or intraperitoneal glucose re-feeding. This effect was dose-dependent and differential, in that ethanol produced no equivalent impairment in glycogen deposition in non-oxidative muscles. Ethanol treatment also selectively promoted glycogenolysis in oxidative muscles in the starved state. There was positive correlation (P < 0.001) between the decrease in glycogen levels in soleus and diaphragm muscles in response to increasing ethanol doses and blood glucose and lactate concentrations after intraperitoneal glucose administration, implying that the basis for the impairment in glycogen synthesis may be diminished glucose availability. The mechanism whereby ethanol may differentially compromise carbohydrate metabolism in oxidative muscles is discussed.

scholarly journals Re-feeding after starvation involves a temporal shift in the control site of glycogen synthesis in rat muscle

1998 ◽  
Vol 329 (2) ◽  
pp. 341-347 ◽  
Author(s):  
P. Anthony JAMES ◽  
B. Carrie FLYNN ◽  
L. Sioned JONES ◽  
T. Norman PALMER ◽  
A. Paul FOURNIER
Keyword(s):  
Skeletal Muscles ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Quadriceps Muscle ◽  
Control Site ◽  
Temporal Shift ◽  
Fed State ◽  
Phosphorylation State ◽  
Glycogen Deposition ◽  
Later Phase

The starved-to-fed transition is accompanied by rapid glycogen deposition in skeletal muscles. On the basis of recent findings [Bräu, Ferreira, Nikolovski, Raja, Palmer and Fournier (1997) Biochem. J. 322, 303-308] that during recovery from exercise there is a shift from a glucose 6-phosphate/phosphorylation-based control of glycogen synthesis to a phosphorylation-based control alone, this paper seeks to establish whether a similar shift occurs in muscle during re-feeding after starvation in the rat. Chow re-feeding after 48 h of starvation resulted in glycogen deposition in all muscles examined (white, red and mixed quadriceps, soleus and diaphragm) to levels higher than those in the fed state. Although the early phase of re-feeding was associated with increases in glucose 6-phosphate levels in all muscles, there was no accompanying increase in the fractional velocity of glycogen synthase except in the white quadriceps muscle. This finding, together with the observation that the fractional velocity of glycogen synthase in most muscles was already high in the starved state, suggests that in the initial phase of glycogen deposition the phosphorylation state of the enzyme may be adequate to support net glycogen synthesis. In the later phase of re-feeding, the progressive decrease in the fractional velocity of glycogen synthase in association with a decrease in the rate of glycogen deposition suggests that glycogen synthesis is controlled primarily by changes in the phosphorylation state of glycogen synthase. In conclusion, this study suggests that there is a temporal shift in the site of control of glycogen synthesis as glycogen deposition progresses during re-feeding after starvation.

scholarly journals Pyrrolidine dithiocarbamate enhances hepatic glycogen synthesis and reduces FoxO1-mediated gene transcription in type 2 diabetic rats

2012 ◽  
Vol 302 (4) ◽  
pp. E409-E416 ◽  
Author(s):  
Tienian Zhu ◽  
Ruijing Zhao ◽  
Lizhong Zhang ◽  
Michel Bernier ◽  
Jiankun Liu
Keyword(s):  
Blood Glucose ◽  
Glycogen Synthesis ◽  
Fasting Blood Glucose ◽  
Diabetic Rats ◽  
Hepatic Glycogen ◽  
Pyrrolidine Dithiocarbamate ◽  
Glycogen Deposition ◽  
Gsk 3Β ◽  
Type 2 Diabetic

The aim of the present study was to examine the effects of pyrrolidine dithiocarbamate (PDTC) on hepatic glycogen synthesis and FoxO1 transcriptional activity in type 2 diabetic rats and the mechanism underlying these effects. Fasting blood glucose and glycogen deposition, together with expressions of two key genes related to gluconeogenesis, were studied in the liver of rats fed a normal diet (NC), high-fat diet (HFD)-induced insulin-resistant rats made type 2 diabetic by a single intraperitoneal injection of streptozotocin (DM), and a DM with intervention of PDTC (DM + PDTC) for 1 wk. The phosphorylation of Akt, GSK-3β, and FoxO1 was assessed in liver extracts of fasted rats by Western blot, whereas indirect immunofluorescence staining was performed to determine the cellular distribution of FoxO1. The DM rats exhibited obvious increases in fasting blood glucose as well as decreased hepatic glycogen content compared with the NC group. Activation of the Akt/GSK-3β pathway and inactivating phosphorylation of FoxO1 were reduced greatly in DM rat livers ( P < 0.01). By contrast, PDTC treatment protected DM rats against high fasting blood glucose and hepatic glycogen deposition loss. PDTC also elicited an increase in Akt/GSK-3β signaling and subsequent inactivation and nuclear export of FoxO1 in DM rat livers, which translated into a significant reduction in the expression of two FoxO1 target genes, phospho enolpyruvate carboxykinase and glucose-6-phosphatase. This study suggests that PDTC enhances hepatic glycogen synthesis, whereas it reduces FoxO1 transcriptional activity in DM 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.

scholarly journals Glycogen synthesis in the perfused liver of adrenalectomized rats

1976 ◽  
Vol 156 (3) ◽  
pp. 585-592 ◽  
Author(s):  
P D Whitton ◽  
D A Hems
Keyword(s):  
Intact Animal ◽  
Glycogen Synthesis ◽  
Hepatic Metabolism ◽  
Hepatic Glycogen ◽  
Perfused Liver ◽  
Short Term ◽  
Glycogen Accumulation ◽  
Glycogen Deposition ◽  
Adrenalectomized Rats

1. A total loss of capacity for net glycogen synthesis was observed in experiments with the perfused liver of starved adrenalectomized rats. 2. This lesion was corrected by insulin or cortisol in vivo (over 2-5h), but not by any agent tested in perfusion. 3. The activity of glycogen synthetase a, and its increase during perfusion, in the presence of glucose plus glucogenic substrates, were proportional to the rate of net glycogen accumulation. 4. This complete inherent loss of capacity for glycogen synthesis after adrenalectomy is greater than any defect in hepatic metabolism yet reported in this situation, and is not explicable by a decrease in the rate of gluconegenesis (which supports glycogen synthesis in the liver of starved rats). The short-term (2-5h) stimulatory effect of glucocorticoids in the intact animal, on hepatic glycogen deposition, may be mediated partly through insulin action, although neither insulin or cortisol appear to act directly on the liver to stimulate glycogen synthesis.

scholarly journals Glycaemic index values for commercially available potatoes in Great Britain

2005 ◽  
Vol 94 (6) ◽  
pp. 917-921 ◽  
Author(s):  
C. Jeya K. Henry ◽  
Helen J. Lightowler ◽  
Caroline M. Strik ◽  
Michael Storey
Keyword(s):  
Blood Glucose ◽  
Great Britain ◽  
Glycaemic Index ◽  
Crossover Design ◽  
Repeated Measure ◽  
Glycaemic Response ◽  
Potato Varieties ◽  
Glycaemic Load ◽  
Wide Range ◽  
Finger Prick

The glycaemic response to eight potato varieties commercially available in Great Britain was compared against a glucose standard in a non-blind, randomised, repeated measure, crossover design trial. Seventeen healthy subjects (three males, fouteen females), mean age 32 (sd 13) years and mean BMI 22·3 (sd 3·6) kg/m2, were recruited to the study. Subjects were served portions of eight potato varieties and a standard food (glucose), on separate occasions, each containing 50 g carbohydrate. Capillary blood glucose was measured from finger-prick samples in fasted subjects (0 min) and at 15, 30, 45, 60, 90 and 120 min after the consumption of each test food. For each potato variety, the glycaemic index (GI) value was calculated geometrically by expressing the incremental area under the blood glucose curve (IAUC) as a percentage of each subject's average IAUC for the standard food. The eight potato varieties exhibited a wide range in GI values from 56 to 94. A trend was seen whereby potatoes with waxy textures produced medium GI values, whilst floury potatoes had high GI values. Considering the widespread consumption of potatoes in Great Britain (933–1086 g per person per week), this information could be used to help lower the overall GI and glycaemic load of the diets of the British population.

scholarly journals Glycaemic potency reduction by coarse grain structure in breads is largely eliminated during normal ingestion

2021 ◽  
pp. 1-27
Author(s):  
Akila SRV ◽  
Suman Mishra ◽  
Allan Hardacre ◽  
Lara Matia-Merino ◽  
Kelvin Goh ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glycaemic Index ◽  
Moderating Effect ◽  
Grain Structure ◽  
Coarse Grain ◽  
White Bread ◽  
Starch Digestion ◽  
Glycaemic Response ◽  
Significant Difference

Abstract The hypothesis that coarse grain particles in breads reduce glycaemic response only if the particles remain intact during ingestion was tested. Three breads were formulated: (1) White bread (WB - reference), (2) 75% of kibbled purple wheat in 25% white bread matrix (PB), (3) a 1:1 mixture of 37.5% kibbled soy beans and 37.5% of kibble purple wheat in 25% white bread matrix (SPB). Each bread was ingested in three forms: unchewed (U), as customarily consumed (C), and homogenized (H). Twelve participants ingested 40 g available carbohydrate portions of each bread in each form, with post prandial blood glucose measured over 120 min. Glycaemic responses to WB were the same regardless of its form when ingested. Unchewed PB had significantly less glycaemic effect than WB, whereas the C and H forms were similar to WB. Based on a glycaemic index (GI) of 70 for WB the GI values for the C, U and H breads respectively were WB: 70.0, 70, 70, PB: 75, 42, 61, SPB: 57, 48, 55 (%) (Least significant difference = 17.43, p <0.05, bold numbers significantly different from WB). The similar glycaemic response to the H and C forms of the breads, and their difference from the U form, showed that the glycaemia-moderating effect of grain structure on starch digestion was lost during customary ingestion of bread. We conclude that kibbled grain structure may not effectively retard starch digestion in breads as normally consumed because it is largely eliminated by ingestive processes including chewing.

Carbohydrate and Protein Supplements, an Effective Means for Maintaining Exercise-Induced Glucose Metabolism Homeostasis

2021 ◽  
Vol 11 (6) ◽  
pp. 1120-1128
Author(s):  
Dingguo Ruan ◽  
Hong Deng ◽  
Xiaoyang Xu
Keyword(s):  
Blood Glucose ◽  
Glucose Metabolism ◽  
Normal Saline ◽  
Glucose Transporter ◽  
Glycogen Synthesis ◽  
Effective Means ◽  
Recovery Period ◽  
Future Application ◽  
Glut 4 ◽  
Exercise Induced

This study aimed to verify the effects of an independently developed carbohydrate and protein (CHO+P) beverage (7.2% oligosaccharide and 1.6% soy-polypeptide) supplement on exerciseinduced glucose metabolism and associated gene expression. Mice received 1 mL/100 g body weight of normal saline (group C; n = 36) or CHO+P (group E; n = 36) at 30 min before an immediately after exercise. Mice without exercise and supplementation served as normal controls (group NC; n = 9). The expression levels related to glucose metabolism were measured at 0, 4, 12, and 24 h after exercise (n = 9 per group). The blood glucose, insulin, and liver glycogen contents in groups C and E were dramatically lower than group NC immediately after exercise. Those in group E were significantly higher than group C, with few differences between the two. Muscle glycogen was restored more quickly when the CHO+P beverage was consumed compared to normal saline. Furthermore, exercise-induced increase in glucose transporter-4 (GLUT-4) mRNA could be depressed by CHO+P supplementation but enhanced in GLUT-4 protein. Interleukin-6 (IL-6) showed a double peak curve in the recovery period, but IL-6 increased again in group E earlier than group C. These findings confirmed that the beverage has significantly improved time in maintaining blood glucose stability, reducing glycogen consumption, accelerating glycogen resynthesis, and repairing injury in rats. This study suggests the future application of this beverage in humans with experimental support and provides a scientific direction for promoting glycogen synthesis and recovery through nutrition.

Does dietary fat cause a dose dependent glycaemic response in youth with type 1 diabetes?

2021 ◽  
Author(s):  
Susan M. O'Connell ◽  
Norma M. A. O'Toole ◽  
Conor N. Cronin ◽  
Chen Saat‐Murphy ◽  
Patrick McElduff ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Dietary Fat ◽  
Glycaemic Response ◽  
Dose Dependent

scholarly journals Dose-Dependent Effects of Recombinant Human Interleukin-6 on Glucose Regulation

1997 ◽  
Vol 82 (12) ◽  
pp. 4167-4170 ◽  
Author(s):  
Constantine Tsigos ◽  
Dimitris A. Papanicolaou ◽  
Ioannis Kyrou ◽  
Ruby Defensor ◽  
Constantine S. Mitsiadis ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Interleukin 6 ◽  
Peak Plasma ◽  
Fasting Blood Glucose ◽  
Peripheral Resistance ◽  
C Peptide ◽  
Inflammatory Stress ◽  
Glucose Levels ◽  
Dose Dependent Fashion ◽  
Dose Dependent

Inflammatory cytokines have metabolic actions that probably contribute to the general adaptation of the organism during infectious or inflammatory stress. To examine the effects of interleukin 6 (IL-6), the main circulating cytokine, on glucose metabolism in man, we performed dose-response studies of recombinant human IL-6 in normal volunteers. Increasing single doses of IL-6 (0.1, 0.3, 1.0, 3.0, and 10.0 mg/Kg BW) were injected sc in 15 healthy male volunteers (3 in each dose) after a 12-h fast. All IL-6 doses were tolerated well and produced no significant adverse effects. We measured the circulating levels of glucose, insulin, C-peptide, and glucagon at baseline and half-hourly over 4 h after the IL-6 injection. Mean peak plasma levels of IL-6 were achieved between 120 and 240 min and were 8, 22, 65, 290, and 4050 pg/mL, respectively, for the 5 doses. After administration of the 2 smaller IL-6 doses, we observed no significant changes in plasma glucose levels, which, because of continued fasting, decreased slightly over time. By 60 min after the 3 higher IL-6 doses, however, the decline in fasting blood glucose was arrested, and glucose levels increased in a dose-dependent fashion. The concurrent levels of plasma insulin and C-peptide were not affected by any IL-6 dose. In contrast, IL-6 caused significant increases in plasma glucagon levels, which peaked between 120 and 150 min after the IL-6 injection. In conclusion, sc IL-6 administration induced dose-dependent increases in fasting blood glucose, probably by stimulating glucagon release and other counteregulatory hormones and/or by inducing peripheral resistance to insulin action.

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