scholarly journals REGULATION OF GLUCOSE STORAGE EXTENDS LIFESPAN AND PROMOTES HEALTHSPAN

2018 ◽  
Vol 2 (suppl_1) ◽  
pp. 74-74
Author(s):  
H Tissenbaum ◽  
Y Seo ◽  
S Kingsley ◽  
G Walker ◽  
M A Mondoux
Keyword(s):  
Glucose Storage

Metabolic Effects of Acute Hyperketonaemia in Man before and during An Hyperinsulinaemic Euglycaemic Clamp

1994 ◽  
Vol 86 (6) ◽  
pp. 677-687 ◽  
Author(s):  
J. Webber ◽  
E. Simpson ◽  
H. Parkin ◽  
I. A. MacDonald
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Glucose Oxidation ◽  
Respiratory Exchange Ratio ◽  
Saline Infusion ◽  
Metabolic Effects ◽  
Whole Body ◽  
Glucose Storage ◽  
Adipose Tissue Lipolysis ◽  
Subcutaneous Abdominal Adipose Tissue

1. The effects of acutely raising blood ketone body levels to those seen after 72 h of starvation were examined in 10 subjects after an overnight fast. Metabolic rate and respiratory exchange ratio were measured with indirect calorimetry before and during an insulin—glucose clamp. Arteriovenous differences were measured across forearm and subcutaneous abdominal adipose tissue. 2. In response to the clamp the respiratory exchange ratio rose from 0.82 to 0.83 during 3-hydroxybutyrate infusion and from 0.83 to 0.94 during control (saline) infusion (P < 0.001). 3. Forearm glucose uptake at the end of the clamp was 4.02 ± 0.95 (3-hydroxybutyrate infusion) and 7.09 ± 1.24 mmol min−1 100 ml−1 forearm (saline infusion). Whole body glucose uptake at the end of the clamp was 72.8 ± 7.9 (3-hydroxybutyrate infusion) and 51.0 ± 3.0 (saline infusion) mmol min−1 kg−1 body weight−1. 4. 3-Hydroxybutyrate infusion reduced the baseline abdominal venous—arterialized venous glycerol difference from 84 ± 28 to 25 ± 12 mmol/l and the non-esterified fatty acid difference from 0.60 ± 0.17 to 0.02 ± 0.09 mmol/l (P < 0.05 versus saline infusion). 5. Hyperketonaemia reduces adipose tissue lipolysis and decreases insulin-mediated forearm glucose uptake. Hyperketonaemia appears to prevent insulin-stimulated glucose oxidation, but does not reduce insulin-mediated glucose storage.

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.

Impairment of glucose disposal by infusion of triglycerides in humans: role of glycemia

1989 ◽  
Vol 256 (6) ◽  
pp. E747-E752 ◽  
Author(s):  
C. P. Felley ◽  
E. M. Felley ◽  
G. D. van Melle ◽  
P. Frascarolo ◽  
E. Jequier ◽  
...  
Keyword(s):  
Glucose Oxidation ◽  
Plasma Free Fatty Acid ◽  
Regulatory Mechanisms ◽  
Glucose Disposal ◽  
Glucose Storage ◽  
Interaction Term ◽  
The Difference ◽  
Total Glucose

The present study was designed to assess the role of hyperglycemia (150 mg/dl) vs. euglycemia (90 mg/dl) on glucose metabolism in vivo during the infusion of a triglyceride emulsion (Intralipid). Seven young healthy volunteers were studied on four occasions using the hyperinsulinemic clamp technique, twice during euglycemia and twice during hyperglycemia, without or with Intralipid. Glucose oxidation (O) was calculated from continuous respiratory exchange measurements, and glucose storage (S) was obtained as the difference between total glucose disposal (M) and O. Two-way analysis of variance with interaction term demonstrated 1) a significant increase for M with hyperglycemia and a decrease with Intralipid; no interaction, and 2) in euglycemia, O/M and S/M occurred in one-to-one ratios; on the other hand, during 150-mg/dl hyperglycemia, the ratio dropped roughly to 1:2. Intralipid had no effect on the ratio, and no interaction could be observed. These results suggest the existence of physiological regulatory mechanisms by which 1) the rise in plasma free fatty acid inhibits both oxidative and nonoxidative glucose disposal, and 2) the rise in glycemia stimulates predominantly nonoxidative glucose disposal.

Energy expenditure after infusion of glucose-based total parenteral nutrition

1987 ◽  
Vol 253 (2) ◽  
pp. E135-E141 ◽  
Author(s):  
K. M. Gil ◽  
J. Askanazi ◽  
D. H. Elwyn ◽  
F. E. Gump ◽  
J. M. Kinney
Keyword(s):  
Energy Expenditure ◽  
Parenteral Nutrition ◽  
Total Parenteral Nutrition ◽  
Resting Energy Expenditure ◽  
Glucose Intake ◽  
Glucose Storage ◽  
Group 2 ◽  
Ree Group ◽  
Thermic Effect ◽  
Group 1

Resting energy expenditure (REE), carbohydrate balance, and lipogenesis were calculated after administration of glucose-based total parenteral nutrition (TPN) to determine whether the thermic effect of glucose is equal to the energy cost of storing the glucose. Estimated cost of storage as glycogen (5.3%) and fat (19%) was compared with measured increases in REE. Patients with malnutrition received 5% dextrose in water and 6 days of TPN with a low (1.2 times REE, group 1) or high (2.0 times REE, group 2) level of glucose intake. Increases in REE by day 6 were 10% (group 1) and 28% (group 2). The theoretical cost of glucose storage as glycogen and fat accounted for approximately 40% of the measured increase in REE in patients in group 2. The thermic effect of TPN (derived from patients in group 1) accounted for most of the balance. The majority of the thermic effect of high levels of glucose infused with TPN can be explained on the basis of the thermic effect of TPN and glucose storage.

The effect of hyperglycemia, hyperinsulinemia, and route of glucose administration on glucose oxidation and glucose storage

Metabolism ◽  
1982 ◽  
Vol 31 (9) ◽  
pp. 922-930 ◽  
Author(s):  
Eric Jacot ◽  
Ralph A. Defronzo ◽  
Eric Jéquier ◽  
Evelyne Maeder ◽  
Jean-Pierre Felber
Keyword(s):  
Glucose Oxidation ◽  
Glucose Administration ◽  
Glucose Storage

Pathways for glucose disposal after meal ingestion in humans

2003 ◽  
Vol 284 (4) ◽  
pp. E716-E725 ◽  
Author(s):  
Hans J. Woerle ◽  
Christian Meyer ◽  
Jean M. Dostou ◽  
Niyaz R. Gosmanov ◽  
Nazmul Islam ◽  
...  
Keyword(s):  
Tritiated Water ◽  
Postprandial Glucose ◽  
Systemic Circulation ◽  
Glucose Disposal ◽  
Indirect Pathway ◽  
Postprandial Period ◽  
Glucose Storage ◽  
Meal Ingestion ◽  
And Storage ◽  
Glycogen Formation

To characterize postprandial glucose disposal more completely, we used the tritiated water technique, a triple-isotope approach (intravenous [3-H3]glucose and [14C]bicarbonate and oral [6,6-2H2]glucose) and indirect calorimetry to assess splanchnic and peripheral glucose disposal, direct and indirect glucose storage, oxidative and nonoxidative glycolysis, and the glucose entering plasma via gluconeogenesis after ingestion of a meal in 11 normal volunteers. During a 6-h postprandial period, a total of ∼98 g of glucose were disposed of. This was more than the glucose contained in the meal (∼78 g) due to persistent endogenous glucose release (∼21 g): splanchnic tissues initially took up ∼23 g, and an additional ∼75 g were removed from the systemic circulation. Direct glucose storage accounted for ∼32 g and glycolysis for ∼66 g (oxidative ∼43 g and nonoxidative ∼23 g). About 11 g of glucose appeared in plasma as a result of gluconeogenesis. If these carbons were wholly from glucose undergoing glycolysis, only ∼12 g would be available for indirect pathway glycogen formation. Our results thus indicate that glycolysis is the main initial postprandial fate of glucose, accounting for ∼66% of overall disposal; oxidation and storage each account for ∼45%. The majority of glycogen is formed via the direct pathway (∼73%).

Overnutrition induced decrease in insulin action for glucose storage: In vivo and in vitro in man

Metabolism ◽  
1986 ◽  
Vol 35 (2) ◽  
pp. 160-165 ◽  
Author(s):  
D.M. Mott ◽  
S. Lillioja ◽  
C. Bogardus
Keyword(s):  
Insulin Action ◽  
Glucose Storage

scholarly journals Glucose storage and oxidation in different degrees of human obesity measured by continuous indirect calorimetry

Diabetologia ◽  
1981 ◽  
Vol 20 (1) ◽  
pp. 39-44 ◽  
Author(s):  
J. -P. Felber ◽  
H. U. Meyer ◽  
B. Curchod ◽  
H. U. Iselin ◽  
J. Rousselle ◽  
...  
Keyword(s):  
Indirect Calorimetry ◽  
Human Obesity ◽  
Glucose Storage

scholarly journals Adaptations to excess choline in insulin resistant and Pcyt2 deficient skeletal muscle

2017 ◽  
Vol 95 (2) ◽  
pp. 223-231 ◽  
Author(s):  
Adrian Taylor ◽  
Laila Cigana Schenkel ◽  
Maiya Yokich ◽  
Marica Bakovic
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Signaling ◽  
Lipid Analysis ◽  
Choline Transport ◽  
Insulin Resistant ◽  
Expression Of Genes ◽  
Metabolic Gene Expression ◽  
Glucose Storage ◽  
Positive Effect ◽  
Deficient Mice

It was hypothesized that choline supplementation in insulin resistant (IR) CTP:phosphoethanolamine cytidylyltransferase deficient (Pcyt2+/−) mice would ameliorate muscle function by remodeling glucose and fatty acid (FA) metabolism. Pcyt2+/− mice either received no treatment or were allowed access to 2 mg/mL choline in drinking water for 4 weeks. Skeletal muscle was harvested from choline treated and untreated mice. Lipid analysis and metabolic gene expression and signaling pathways were compared between untreated Pcyt2+/− mice, treated Pcyt2+/− mice, and Pcyt2+/+ mice. The major positive effect of choline supplementation on IR muscle was the reduction of glucose utilization for FA and triglyceride (TAG) synthesis and increased muscle glucose storage as glycogen. Choline reduced the expression of genes for FA and TAG formation (Scd1, Fas, Srebp1c, Dgat1/2), upregulated the genes for FA oxidation (Cpt1, Pparα, Pgc1α), and had minor effects on phospholipid and lipolysis genes. Pcyt2+/− muscle had reduced insulin signaling (IRS1), autophagy (LC3), and choline transport (CTL1) proteins that were restored by choline treatment. Additionally, choline activated AMPK and Akt while inhibiting mTORC1 phosphorylation. These data established that choline supplementation could restore muscle glucose metabolism by reducing lipogenesis and improving mitochondrial and intracellular signaling for protein and energy metabolism in insulin resistant Pcyt2 deficient mice.

Effect of a 3-day fast on glucose storage and oxidation in obese hyperinsulinemic diabetics

Metabolism ◽  
1981 ◽  
Vol 30 (2) ◽  
pp. 184-189 ◽  
Author(s):  
J.-P. Felber ◽  
H.U. Meyer ◽  
B. Curchod ◽  
E. Maeder ◽  
P. Pahud ◽  
...  
Keyword(s):  
Glucose Storage
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