scholarly journals Effect of muscle glycogen depletion on in vivo insulin action in man.

1983 ◽  
Vol 72 (5) ◽  
pp. 1605-1610 ◽  
Author(s):  
C Bogardus ◽  
P Thuillez ◽  
E Ravussin ◽  
B Vasquez ◽  
M Narimiga ◽  
...  
Keyword(s):  
Muscle Glycogen ◽  
Insulin Action ◽  
Glycogen Depletion

scholarly journals Muscle glycogen and metabolic regulation

2004 ◽  
Vol 63 (2) ◽  
pp. 217-220 ◽  
Author(s):  
Mark Hargreaves
Keyword(s):  
Muscle Glycogen ◽  
Insulin Action ◽  
Metabolic Regulation ◽  
Strenuous Exercise ◽  
Glycogen Depletion ◽  
Excitation Contraction Coupling ◽  
Glycogen Resynthesis ◽  
Contraction Coupling ◽  
Cellular Processes ◽  
Exercise Induced

Muscle glycogen is an important fuel for contracting skeletal muscle during prolonged strenuous exercise, and glycogen depletion has been implicated in muscle fatigue. It is also apparent that glycogen availability can exert important effects on a range of metabolic and cellular processes. These processes include carbohydrate, fat and protein metabolism during exercise, post-exercise glycogen resynthesis, excitation–contraction coupling, insulin action and gene transcription. For example, low muscle glycogen is associated with reduced muscle glycogenolysis, increased glucose and NEFA uptake and protein degradation, accelerated glycogen resynthesis, impaired excitation–contraction coupling, enhanced insulin action and potentiation of the exercise-induced increases in transcription of metabolic genes. Future studies should identify the mechanisms underlying, and the functional importance of, the association between glycogen availability and these processes.

Epinephrine-induced in vivo muscle glycogen depletion enhances insulin sensitivity of glucose transport

1994 ◽  
Vol 76 (5) ◽  
pp. 2054-2058 ◽  
Author(s):  
L. A. Nolte ◽  
E. A. Gulve ◽  
J. O. Holloszy
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Transport ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Effective Concentration ◽  
Prior Exposure ◽  
Transport Activity ◽  
Glycogen Depletion ◽  
Adrenergic Antagonist

Muscle glycogen depletion by means of exercise is associated with increased insulin-stimulated glucose transport activity. To determine whether reduction in muscle glycogen content independent of muscle contractions would increase glucose transport activity, rats were injected with epinephrine (20 micrograms/100 g body wt) or saline. Two hours later, epitrochlearis muscles were removed, washed thoroughly to remove epinephrine, and assayed for glucose transport activity with 3-O-methyl-D-glucose (3-MG). Muscle adenosine 3′,5′-cyclic monophosphate concentration was elevated 441% in muscles frozen immediately after removal from epinephrine-injected rats but had returned to control levels by the time 3-MG transport was measured. Prior exposure to epinephrine resulted in depletion of muscle glycogen [from 18.6 +/- 1.4 to 11.0 +/- 0.1 (SE) mumol glucose units/g wet wt] and a small increase in basal glucose transport activity (from 0.13 +/- 0.02 to 0.24 +/- 0.04 mumol 3-MG.ml-1 x 10 min-1, P < 0.05). A submaximally effective insulin concentration (30 microU/ml) induced a 70% greater increase in 3-MG transport in epinephrine-treated muscles than in controls (0.57 +/- 0.09 and 0.34 +/- 0.04 mumol.ml-1 x 10 min-1, respectively, P < 0.001). Response to a maximally effective concentration of insulin was unaltered by prior exposure to epinephrine. When epinephrine-induced glycogen depletion was prevented by prior injection with the beta-adrenergic antagonist propranolol, glucose transport activity was no longer enhanced by epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

In vivo deactivation of peripheral, hepatic, and pancreatic insulin action in man

Diabetes ◽  
1982 ◽  
Vol 31 (10) ◽  
pp. 929-936 ◽  
Author(s):  
R. S. Gray ◽  
J. A. Scarlett ◽  
J. Griffin ◽  
J. M. Olefsky ◽  
O. G. Kolterman
Keyword(s):  
Insulin Action ◽  
Pancreatic Insulin

Distribution of in vivo insulin action in Pima Indians as mixture of three normal distributions

Diabetes ◽  
1989 ◽  
Vol 38 (11) ◽  
pp. 1423-1432 ◽  
Author(s):  
C. Bogardus ◽  
S. Lillioja ◽  
B. L. Nyomba ◽  
F. Zurlo ◽  
B. Swinburn ◽  
...  
Keyword(s):  
Insulin Action ◽  
Pima Indians ◽  
Normal Distributions

scholarly journals Effects of Nutrient Intake Timing on Post-Exercise Glycogen Accumulation and its Related Signaling Pathways in Mouse Skeletal Muscle

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2555 ◽  
Author(s):  
Takahashi ◽  
Matsunaga ◽  
Banjo ◽  
Takahashi ◽  
Sato ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Nutrient Intake ◽  
Matched Control ◽  
Control Group ◽  
Glycogen Depletion ◽  
Post Exercise ◽  
Glycogen Accumulation ◽  
Matched Control Group ◽  
Significant Difference

We investigated the effects of nutrient intake timing on glycogen accumulation and its related signals in skeletal muscle after an exercise that did not induce large glycogen depletion. Male ICR mice ran on a treadmill at 25 m/min for 60 min under a fed condition. Mice were orally administered a solution containing 1.2 mg/g carbohydrate and 0.4 mg/g protein or water either immediately (early nutrient, EN) or 180 min (late nutrient, LN) after the exercise. Tissues were harvested at 30 min after the oral administration. No significant difference in blood glucose or plasma insulin concentrations was found between the EN and LN groups. The plantaris muscle glycogen concentration was significantly (p < 0.05) higher in the EN group—but not in the LN group—compared to the respective time-matched control group. Akt Ser473 phosphorylation was significantly higher in the EN group than in the time-matched control group (p < 0.01), while LN had no effect. Positive main effects of time were found for the phosphorylations in Akt substrate of 160 kDa (AS160) Thr642 (p < 0.05), 5'-AMP-activated protein kinase (AMPK) Thr172 (p < 0.01), and acetyl-CoA carboxylase Ser79 (p < 0.01); however, no effect of nutrient intake was found for these. We showed that delayed nutrient intake could not increase muscle glycogen after endurance exercise which did not induce large glycogen depletion. The results also suggest that post-exercise muscle glycogen accumulation after nutrient intake might be partly influenced by Akt activation. Meanwhile, increased AS160 and AMPK activation by post-exercise fasting might not lead to glycogen accumulation.

Effects of keishi-ka-jutsubu-to (traditional herbal medicine: Gui-zhi-jia-shu-fu-tang) on in vivo insulin action in streptozotocin-induced diabetic rats

Life Sciences ◽  
2003 ◽  
Vol 73 (21) ◽  
pp. 2687-2701 ◽  
Author(s):  
Bolin Qin ◽  
Masaru Nagasaki ◽  
Ming Ren ◽  
Gustavo Bajotto ◽  
Yoshiharu Oshida ◽  
...  
Keyword(s):  
Herbal Medicine ◽  
Insulin Action ◽  
Diabetic Rats ◽  
Traditional Herbal Medicine

scholarly journals Minimal impact of age and housing temperature on the metabolic phenotype of Acc2−/− mice

2015 ◽  
Vol 228 (3) ◽  
pp. 127-134 ◽  
Author(s):  
Amanda E Brandon ◽  
Ella Stuart ◽  
Simon J Leslie ◽  
Kyle L Hoehn ◽  
David E James ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Composition ◽  
Energy Expenditure ◽  
Glucose Tolerance ◽  
Fat Mass ◽  
Knockout Mice ◽  
Muscle Glycogen ◽  
Insulin Action ◽  
Metabolic Phenotype ◽  
Whole Body

An important regulator of fatty acid oxidation (FAO) is the allosteric inhibition of CPT-1 by malonyl-CoA produced by the enzyme acetyl-CoA carboxylase 2 (ACC2). Initial studies suggested that deletion of Acc2 (Acacb) increased fat oxidation and reduced adipose tissue mass but in an independently generated strain of Acc2 knockout mice we observed increased whole-body and skeletal muscle FAO and a compensatory increase in muscle glycogen stores without changes in glucose tolerance, energy expenditure or fat mass in young mice (12–16 weeks). The aim of the present study was to determine whether there was any effect of age or housing at thermoneutrality (29 °C; which reduces total energy expenditure) on the phenotype of Acc2 knockout mice. At 42–54 weeks of age, male WT and Acc2−/− mice had similar body weight, fat mass, muscle triglyceride content and glucose tolerance. Consistent with younger Acc2−/− mice, aged Acc2−/− mice showed increased whole-body FAO (24 h average respiratory exchange ratio=0.95±0.02 and 0.92±0.02 for WT and Acc2−/− mice respectively, P<0.05) and skeletal muscle glycogen content (+60%, P<0.05) without any detectable change in whole-body energy expenditure. Hyperinsulinaemic–euglycaemic clamp studies revealed no difference in insulin action between groups with similar glucose infusion rates and tissue glucose uptake. Housing Acc2−/− mice at 29 °C did not alter body composition, glucose tolerance or the effects of fat feeding compared with WT mice. These results confirm that manipulation of Acc2 may alter FAO in mice, but this has little impact on body composition or insulin action.

scholarly journals Endothelial insulin receptors differentially control insulin signaling kinetics in peripheral tissues and brain of mice

2017 ◽  
Vol 114 (40) ◽  
pp. E8478-E8487 ◽  
Author(s):  
Masahiro Konishi ◽  
Masaji Sakaguchi ◽  
Samuel M. Lockhart ◽  
Weikang Cai ◽  
Mengyao Ella Li ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Cells ◽  
Food Intake ◽  
Insulin Signaling ◽  
Insulin Action ◽  
Insulin Receptors ◽  
Brain Regions ◽  
Peripheral Tissues ◽  
Systemic Insulin Resistance

Insulin receptors (IRs) on endothelial cells may have a role in the regulation of transport of circulating insulin to its target tissues; however, how this impacts on insulin action in vivo is unclear. Using mice with endothelial-specific inactivation of the IR gene (EndoIRKO), we find that in response to systemic insulin stimulation, loss of endothelial IRs caused delayed onset of insulin signaling in skeletal muscle, brown fat, hypothalamus, hippocampus, and prefrontal cortex but not in liver or olfactory bulb. At the level of the brain, the delay of insulin signaling was associated with decreased levels of hypothalamic proopiomelanocortin, leading to increased food intake and obesity accompanied with hyperinsulinemia and hyperleptinemia. The loss of endothelial IRs also resulted in a delay in the acute hypoglycemic effect of systemic insulin administration and impaired glucose tolerance. In high-fat diet-treated mice, knockout of the endothelial IRs accelerated development of systemic insulin resistance but not food intake and obesity. Thus, IRs on endothelial cells have an important role in transendothelial insulin delivery in vivo which differentially regulates the kinetics of insulin signaling and insulin action in peripheral target tissues and different brain regions. Loss of this function predisposes animals to systemic insulin resistance, overeating, and obesity.

Insulin promotes glycogen synthesis in the absence of GSK3 phosphorylation in skeletal muscle

2008 ◽  
Vol 294 (1) ◽  
pp. E28-E35 ◽  
Author(s):  
Michale Bouskila ◽  
Michael F. Hirshman ◽  
Jørgen Jensen ◽  
Laurie J. Goodyear ◽  
Kei Sakamoto
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Wild Type ◽  
Muscle Glycogen Synthesis ◽  
Mutant Forms

Insulin promotes dephosphorylation and activation of glycogen synthase (GS) by inactivating glycogen synthase kinase (GSK) 3 through phosphorylation. Insulin also promotes glucose uptake and glucose 6-phosphate (G-6- P) production, which allosterically activates GS. The relative importance of these two regulatory mechanisms in the activation of GS in vivo is unknown. The aim of this study was to investigate if dephosphorylation of GS mediated via GSK3 is required for normal glycogen synthesis in skeletal muscle with insulin. We employed GSK3 knockin mice in which wild-type GSK3α and -β genes are replaced with mutant forms (GSK3α/βS21A/S21A/S9A/S9A), which are nonresponsive to insulin. Although insulin failed to promote dephosphorylation and activation of GS in GSK3α/βS21A/S21A/S9A/S9Amice, glycogen content in different muscles from these mice was similar compared with wild-type mice. Basal and epinephrine-stimulated activity of muscle glycogen phosphorylase was comparable between wild-type and GSK3 knockin mice. Incubation of isolated soleus muscle in Krebs buffer containing 5.5 mM glucose in the presence or absence of insulin revealed that the levels of G-6- P, the rate of [14C]glucose incorporation into glycogen, and an increase in total glycogen content were similar between wild-type and GSK3 knockin mice. Injection of glucose containing 2-deoxy-[3H]glucose and [14C]glucose also resulted in similar rates of muscle glucose uptake and glycogen synthesis in vivo between wild-type and GSK3 knockin mice. These results suggest that insulin-mediated inhibition of GSK3 is not a rate-limiting step in muscle glycogen synthesis in mice. This suggests that allosteric regulation of GS by G-6- P may play a key role in insulin-stimulated muscle glycogen synthesis in vivo.

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