scholarly journals Reciprocity Between Skeletal Muscle AMPK Deletion and Insulin Action in Diet-Induced Obese Mice

Diabetes ◽  
2020 ◽  
Vol 69 (8) ◽  
pp. 1636-1649
Author(s):  
Louise Lantier ◽  
Ashley S. Williams ◽  
Ian M. Williams ◽  
Amanda Guerin ◽  
Deanna P. Bracy ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Action ◽  
Obese Mice

scholarly journals Scriptaid enhances skeletal muscle insulin action and cardiac function in obese mice

2017 ◽  
Vol 19 (7) ◽  
pp. 936-943 ◽  
Author(s):  
Vidhi Gaur ◽  
Timothy Connor ◽  
Kylie Venardos ◽  
Darren C. Henstridge ◽  
Sheree D. Martin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Function ◽  
Insulin Action ◽  
Obese Mice ◽  
Muscle Insulin Action

Expression of nitric oxide synthase in skeletal muscle: a novel role for nitric oxide as a modulator of insulin action

Diabetes ◽  
1997 ◽  
Vol 46 (11) ◽  
pp. 1691-1700 ◽  
Author(s):  
S. Kapur ◽  
S. Bedard ◽  
B. Marcotte ◽  
C. H. Cote ◽  
A. Marette
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Insulin Action ◽  
Oxide Synthase

Insulin Action on Glucose Transport in Isolated Skeletal Muscle from Patients with Liver Cirrhosis

1994 ◽  
Vol 29 (1) ◽  
pp. 71-76 ◽  
Author(s):  
U. Johansson ◽  
L. S. Eriksson ◽  
D. Galuska ◽  
J. R. Zierath ◽  
H. Wallberg-henriksson
Keyword(s):  
Skeletal Muscle ◽  
Liver Cirrhosis ◽  
Glucose Transport ◽  
Insulin Action

Na+,K+-ATPase enzyme units in skeletal muscle from lean and obese mice

1978 ◽  
Vol 80 (2) ◽  
pp. 398-404 ◽  
Author(s):  
Ming Huey Lin ◽  
Dale R. Romsos ◽  
Tai Akera ◽  
Gilbert A. Leveille
Keyword(s):  
Skeletal Muscle ◽  
Obese Mice

Does impaired mitochondrial function affect insulin signaling and action in cultured human skeletal muscle cells?

2008 ◽  
Vol 294 (1) ◽  
pp. E97-E102 ◽  
Author(s):  
Audrey E. Brown ◽  
Matthias Elstner ◽  
Stephen J. Yeaman ◽  
Douglass M. Turnbull ◽  
Mark Walker
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
Mitochondrial Respiration ◽  
Respiratory Function ◽  
Insulin Action ◽  
Human Skeletal Muscle ◽  
Human Skeletal Muscle Cells ◽  
Basal Glucose Uptake

Insulin-resistant type 2 diabetic patients have been reported to have impaired skeletal muscle mitochondrial respiratory function. A key question is whether decreased mitochondrial respiration contributes directly to the decreased insulin action. To address this, a model of impaired cellular respiratory function was established by incubating human skeletal muscle cell cultures with the mitochondrial inhibitor sodium azide and examining the effects on insulin action. Incubation of human skeletal muscle cells with 50 and 75 μM azide resulted in 48 ± 3% and 56 ± 1% decreases, respectively, in respiration compared with untreated cells mimicking the level of impairment seen in type 2 diabetes. Under conditions of decreased respiratory chain function, insulin-independent (basal) glucose uptake was significantly increased. Basal glucose uptake was 325 ± 39 pmol/min/mg (mean ± SE) in untreated cells. This increased to 669 ± 69 and 823 ± 83 pmol/min/mg in cells treated with 50 and 75 μM azide, respectively (vs. untreated, both P < 0.0001). Azide treatment was also accompanied by an increase in basal glycogen synthesis and phosphorylation of AMP-activated protein kinase. However, there was no decrease in glucose uptake following insulin exposure, and insulin-stimulated phosphorylation of Akt was normal under these conditions. GLUT1 mRNA expression remained unchanged, whereas GLUT4 mRNA expression increased following azide treatment. In conclusion, under conditions of impaired mitochondrial respiration there was no evidence of impaired insulin signaling or glucose uptake following insulin exposure in this model system.

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.

Interactions between insulin and exercise

2021 ◽  
Vol 478 (21) ◽  
pp. 3827-3846
Author(s):  
Erik A. Richter ◽  
Lykke Sylow ◽  
Mark Hargreaves
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Insulin Action ◽  
Regular Exercise ◽  
Fuel Storage ◽  
Storage Effects ◽  
Glucose Storage ◽  
Glycogen Stores

The interaction between insulin and exercise is an example of balancing and modifying the effects of two opposing metabolic regulatory forces under varying conditions. While insulin is secreted after food intake and is the primary hormone increasing glucose storage as glycogen and fatty acid storage as triglycerides, exercise is a condition where fuel stores need to be mobilized and oxidized. Thus, during physical activity the fuel storage effects of insulin need to be suppressed. This is done primarily by inhibiting insulin secretion during exercise as well as activating local and systemic fuel mobilizing processes. In contrast, following exercise there is a need for refilling the fuel depots mobilized during exercise, particularly the glycogen stores in muscle. This process is facilitated by an increase in insulin sensitivity of the muscles previously engaged in physical activity which directs glucose to glycogen resynthesis. In physically trained individuals, insulin sensitivity is also higher than in untrained individuals due to adaptations in the vasculature, skeletal muscle and adipose tissue. In this paper, we review the interactions between insulin and exercise during and after exercise, as well as the effects of regular exercise training on insulin action.

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