Effect of thyroid hormones on oxidative and nonoxidative glucose metabolism in humans

1988 ◽  
Vol 255 (2) ◽  
pp. E146-E152 ◽  
Author(s):  
M. J. Muller ◽  
K. J. Acheson ◽  
E. Jequier ◽  
A. G. Burger
Keyword(s):  
Glucose Metabolism ◽  
Thyroid Hormones ◽  
Lipid Oxidation ◽  
Healthy Subjects ◽  
Insulin Infusion ◽  
Glucose Disposal ◽  
Similar Extent ◽  
Before And After ◽  
Glucose Storage ◽  
Basal Energy Expenditure

The glucoregulatory function of thyroid hormones was investigated in six healthy subjects before and after 14 day 3,5,3',5'-tetraiodothyronine (T4) treatment (300 micrograms/day) using a sequential clamp protocol for 5 h at euglycemia (0–2 h) and hyperglycemia (165 mg/dl, 2–5 h) and different insulin infusion rates (1.0 for 0–3.5 h and 6.5 mU.kg-1.min-1, for 3.5–5 h). T4 treatment increased basal energy expenditure (+8%), glucose disposal (+31%), and oxidation (+87%) but decreased nonoxidative glucose metabolism (-30%) and was without effect on lipid oxidation. During the euglycemic clamp, T4 treatment enhanced insulin-induced glucose disposal (+16%), glucose oxidation (+34%), and inhibition of lipid oxidation (-66 vs. -40%); nonoxidative glucose metabolism was stimulated to a similar extent before and after T4. During hyperglycemia, 3,5,3'-triiodothyronine (T3) did not affect glucose disposal but increased carbohydrate-induced lipogenesis at both insulin infusion rates. We conclude that T4 treatment promotes glucose disposal and oxidation, T3 decreases noninsulin-mediated glucose storage but does not antagonize insulin action.

Effects of puberty and diabetes on metabolism of insulin-sensitive fuels

1994 ◽  
Vol 266 (6) ◽  
pp. E885-E891 ◽  
Author(s):  
S. Caprio ◽  
G. Cline ◽  
S. Boulware ◽  
C. Permanente ◽  
G. I. Shulman ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Lipid Oxidation ◽  
Insulin Infusion ◽  
Plasma Free Fatty Acid ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Healthy Controls ◽  
Oxidation Rates ◽  
Acid Protein ◽  
Insulin Dependent

Insulin's ability to stimulate glucose metabolism is reduced during normal puberty; these changes are exaggerated in adolescents with insulin-dependent diabetes mellitus (IDDM). Because the effects of puberty and IDDM on the other actions of insulin have not been established, we studied leucine kinetics (using [1-13C]leucine) and fat metabolism during euglycemic hyperinsulinemia (20 mU.m2.min-1) for 3 h in eight healthy and nine IDDM (HbA1 14 +/- 2%) adolescents and six healthy young adult controls. IDDM subjects received overnight low-dose insulin infusion to normalize fasting glucose. Basal and steady-state insulin values (approximately 240 pM) during the study were similar in all three groups. Insulin-stimulated glucose metabolism was reduced by 40% in healthy adolescents vs. adults (P < 0.05) and by an additional 40% in poorly controlled IDDM (P < 0.05 vs, normal adolescents). Although basal glucose and lipid oxidation rates (measured by indirect calorimetry) were similar in all three groups, when insulin was infused, glucose oxidation increased and lipid oxidation decreased only in the two nondiabetic groups. Similarly, insulin significantly reduced plasma free fatty acid levels only in the nondiabetics. Basal leucine flux (an index of protein degradation) was similar in healthy controls but was markedly increased in IDDM adolescents. Despite similar increments in plasma insulin during the clamp, leucine flux remained higher in IDDM adolescents than in healthy controls. Basal leucine oxidation rates were also increased in IDDM subjects compared with nondiabetic groups and declined to a lesser extent during insulin infusion. We conclude that insulin resistance of puberty is selective for glucose metabolism, sparing amino acid/protein metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Dietary palmitate and oleate differently modulate insulin sensitivity in human skeletal muscle

Diabetologia ◽  
2021 ◽  
Author(s):  
Theresia Sarabhai ◽  
Chrysi Koliaki ◽  
Lucia Mastrototaro ◽  
Sabine Kahl ◽  
Dominik Pesta ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Insulin Signalling ◽  
Whole Body ◽  
Glucose Disposal ◽  
Diabetes Research ◽  
German Research Foundation ◽  
Development Fund ◽  
Before And After

Abstract Aims/hypothesis Energy-dense nutrition generally induces insulin resistance, but dietary composition may differently affect glucose metabolism. This study investigated initial effects of monounsaturated vs saturated lipid meals on basal and insulin-stimulated myocellular glucose metabolism and insulin signalling. Methods In a randomised crossover study, 16 lean metabolically healthy volunteers received single meals containing safflower oil (SAF), palm oil (PAL) or vehicle (VCL). Whole-body glucose metabolism was assessed from glucose disposal (Rd) before and during hyperinsulinaemic–euglycaemic clamps with d-[6,6-2H2]glucose. In serial skeletal muscle biopsies, subcellular lipid metabolites and insulin signalling were measured before and after meals. Results SAF and PAL raised plasma oleate, but only PAL significantly increased plasma palmitate concentrations. SAF and PAL increased myocellular diacylglycerol and activated protein kinase C (PKC) isoform θ (p < 0.05) but only PAL activated PKCɛ. Moreover, PAL led to increased myocellular ceramides along with stimulated PKCζ translocation (p < 0.05 vs SAF). During clamp, SAF and PAL both decreased insulin-stimulated Rd (p < 0.05 vs VCL), but non-oxidative glucose disposal was lower after PAL compared with SAF (p < 0.05). Muscle serine1101-phosphorylation of IRS-1 was increased upon SAF and PAL consumption (p < 0.05), whereas PAL decreased serine473-phosphorylation of Akt more than SAF (p < 0.05). Conclusions/interpretation Lipid-induced myocellular insulin resistance is likely more pronounced with palmitate than with oleate and is associated with PKC isoforms activation and inhibitory insulin signalling. Trial registration ClinicalTrials.gov.NCT01736202. Funding German Federal Ministry of Health, Ministry of Culture and Science of the State North Rhine-Westphalia, German Federal Ministry of Education and Research, European Regional Development Fund, German Research Foundation, German Center for Diabetes Research. Graphical abstract

Increased insulin receptor signaling and glycogen synthase activity contribute to the synergistic effect of exercise on insulin action

2003 ◽  
Vol 95 (6) ◽  
pp. 2519-2529 ◽  
Author(s):  
Christine Y. Christ-Roberts ◽  
Thongchai Pratipanawatr ◽  
Wilailak Pratipanawatr ◽  
Rachele Berria ◽  
Renata Belfort ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
Insulin Infusion ◽  
Glycogen Synthase ◽  
Whole Body ◽  
Glucose Disposal ◽  
Phosphatidylinositol 3 Kinase ◽  
Insulin Stimulation ◽  
Glucose Storage ◽  
Exercise Induced ◽  
Phosphatidylinositol 3

The purpose of this study was to determine the factors contributing to the ability of exercise to enhance insulin-stimulated glucose disposal. Sixteen insulin-resistant nondiabetic and seven Type 2 diabetic subjects underwent two hyperinsulinemic (40 mU · m-2 · min-1) clamps, once without and once with concomitant exercise at 70% peak O2 consumption. Exercise was begun at the start of insulin infusion and was performed for 30 min. Biopsies of the vastus lateralis were performed before and after 30 min of insulin infusion (immediately after cessation of exercise). Exercise synergistically increased insulin-stimulated glucose disposal in nondiabetic [from 4.6 ± 0.4 to 9.5 ± 0.8 mg · kg fat-free mass (FFM)-1 · min-1] and diabetic subjects (from 4.3 ± 1.0 to 7.9 ± 0.7 mg · kg FFM-1 · min-1) subjects. The rate of glucose disposal also was significantly greater in each group after cessation of exercise. Exercise enhanced insulin-stimulated increases in glycogen synthase fractional velocity in control (from 0.07 ± 0.02 to 0.22 ± 0.05, P < 0.05) and diabetic (from 0.08 ± 0.03 to 0.15 ± 0.03, P < 0.01) subjects. Exercise also enhanced insulin-stimulated glucose storage (glycogen synthesis) in nondiabetic (2.9 ± 0.9 vs. 4.9 ± 1.1 mg · kg FFM-1 · min-1) and diabetic (1.7 ± 0.5 vs. 4.2 ± 0.8 mg · kg FFM-1 · min-1) subjects. Increased glucose storage accounted for the increase in whole body glucose disposal when exercise was performed during insulin stimulation in both groups; effects of exercise were correlated with enhancement of glucose disposal and glucose storage ( r = 0.93, P < 0.001). Exercise synergistically enhanced insulin-stimulated insulin receptor substrate 1-associated phosphatidylinositol 3-kinase activity ( P < 0.05) and Akt Ser473 phosphorylation ( P < 0.05) in nondiabetic subjects but had little effect in diabetic subjects. The data indicate that exercise, performed in conjunction with insulin infusion, synergistically increases insulin-stimulated glucose disposal compared with insulin alone. In nondiabetic and diabetic subjects, increased glycogen synthase activation is likely to be involved, in part, in this effect. In nondiabetic, but not diabetic, subjects, exercise-induced enhancement of insulin stimulation of the phosphatidylinositol 3-kinase pathway is also likely to be involved in the exercise-induced synergistic enhancement of glucose disposal.

Platelet and adipocyte thermogenesis in hypothyroid patients: a microcalorimetric study

1985 ◽  
Vol 108 (3) ◽  
pp. 361-366 ◽  
Author(s):  
Stig Valdemarsson ◽  
Birger Fagher ◽  
Pavo Hedner ◽  
Mario Monti ◽  
Peter Nilsson-Ehle
Keyword(s):  
Thyroid Hormones ◽  
Heat Production ◽  
Healthy Subjects ◽  
Mean Value ◽  
Metabolic Effects ◽  
Adipocyte Size ◽  
Before And After ◽  
The Mean ◽  
Hypothyroid Patients ◽  
Adequate Method

Abstract. Direct microcalorimetry was used for measurements of heat production in cell suspensions of platelets and adipocytes, obtained from hypothyroid patients before and after 3 months on full l-thyroxine substitution. Platelet heat production was significantly lower than normal before treatment and increased in all 10 patients studied; the mean value increased from 51.3 ± 1.6 fW/cell before to 57.1 ± 1.8 fW/cell after therapy (P< 0.001). Similarily, adipocyte heat production was initially significantly lower than normal and increased during treatment in all 6 patients investigated. The mean value for heat production per adipocyte was 18.8 ± 1.7 pW/cell before and 32.4 ± 2.5 pW/cell after therapy (P < 0.025), which is still below the level recorded in lean healthy subjects. The adipocyte size did not change significantly. The increase in adipocyte heat production was correlated to the increase in S-triiodothyronine levels (r = 0.84, P <0.05). In hypothyroidism, the total metabolic activity seems to be comparatively more reduced in adipocytes than in platelets. A difference may exist between these cells with regard to recovery of normal metabolic acitivity during treatment for hypothyroidism. Direct microcalorimetry appears to be an adequate method for monitoring net metabolic effects of thyroid hormones in these cells.

scholarly journals Oxyntomodulin ameliorates glucose intolerance in mice fed a high-fat diet

2008 ◽  
Vol 294 (1) ◽  
pp. E142-E147 ◽  
Author(s):  
Edwin T. Parlevliet ◽  
Annemieke C. Heijboer ◽  
Janny P. Schröder-van der Elst ◽  
Louis M. Havekes ◽  
Johannes A. Romijn ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Insulin Action ◽  
Insulin Infusion ◽  
Glucose Production ◽  
Tolerance Test ◽  
Glucose Disposal ◽  
Insulin Levels ◽  
Insulin Resistant

We evaluated the acute effects of OXM on glucose metabolism in diet-induced insulin-resistant male C57Bl/6 mice. To determine the effects on glucose tolerance, mice were intraperitoneally injected with OXM (0.75, 2.5, or 7.5 nmol) or vehicle prior to an ip glucose tolerance test. OXM (0.75 nmol/h) or vehicle was infused during a hyperinsulinemic euglycemic clamp to quantify insulin action on glucose production and disposal. OXM dose-dependently improved glucose tolerance as estimated by AUC for glucose (OXM: 7.5 nmol, 1,564 ± 460, P < 0.01; 2.5 nmol, 1,828 ± 684, P < 0.01; 0.75 nmol, 2,322 ± 303, P < 0.05; control: 2,790 ± 222 mmol·l−1·120 min). Insulin levels in response to glucose administration were higher in 7.5 nmol OXM-treated animals compared with controls. In basal clamp conditions, OXM increased EGP (82.2 ± 14.7 vs. 39.9 ± 5.7 μmol·min−1·kg−1, P < 0.001). During insulin infusion, insulin levels were twice as high in OXM-treated mice compared with controls (10.6 ± 2.8 vs. 4.4 ± 2.2 ng/ml, P < 0.01). Consequently, glucose infusion rate (118.6 ± 30.8 vs. 38.8 ± 26.4 μl/h, P < 0.001) and glucose disposal (88.1 ± 13.0 vs. 45.2 ± 6.9 μmol·min−1·kg−1, P < 0.001) were enhanced in mice that received OXM. In addition, glucose production was more suppressed during OXM infusion (35.7 ± 15.5 vs. 15.8 ± 11.4% inhibition, P < 0.05). However, if these data were expressed per unit concentration of circulating insulin, OXM did not affect insulin action on glucose disposal and production. These results indicate that OXM beneficially affects glucose metabolism in diet-induced insulin-resistant C57Bl/6 mice. It ameliorates glucose intolerance, most likely because it elevates glucose-induced plasma insulin concentrations. OXM does not appear to impact on insulin action.

Mechanisms for abnormal postprandial glucose metabolism in type 2 diabetes

2006 ◽  
Vol 290 (1) ◽  
pp. E67-E77 ◽  
Author(s):  
Hans J. Woerle ◽  
Ervin Szoke ◽  
Christian Meyer ◽  
Jean M. Dostou ◽  
Steven D. Wittlin ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Postprandial Glucose ◽  
Postprandial Hyperglycemia ◽  
Glucose Disposal ◽  
Glucose Release ◽  
Isotope Technique ◽  
Glucose Storage ◽  
And Storage

To assess mechanisms for postprandial hyperglycemia, we used a triple-isotope technique ([\3-3H]glucose and [14C]bicarbonate and oral [6,6-dideutero]glucose iv) and indirect calorimetry to compare components of glucose release and pathways for glucose disposal in 26 subjects with type 2 diabetes and 15 age-, weight-, and sex-matched normal volunteers after a standard meal. The results were as follows: 1) diabetic subjects had greater postprandial glucose release ( P < 0.001) because of both increased endogenous and meal-glucose release; 2) the greater endogenous glucose release ( P < 0.001) was due to increased gluconeogenesis ( P < 0.001) and glycogenolysis ( P = 0.01); 3) overall tissue glucose uptake, glycolysis, and storage were comparable in both groups ( P > 0.3); 4) glucose clearance ( P < 0.001) and oxidation ( P = 0.004) were reduced, whereas nonoxidative glycolysis was increased ( P = 0.04); and 5) net splanchnic glucose storage was reduced by ∼45% ( P = 0.008) because of increased glycogen cycling ( P = 0.03). Thus in type 2 diabetes, postprandial hyperglycemia is primarily due to increased glucose release; hyperglycemia overcomes the effects of impaired insulin secretion and sensitivity on glucose transport, but intracellular defects persist so that pathways of glucose metabolism are abnormal and glucose is shunted away from normal sites of storage (e.g., liver and muscle) into other tissues.

scholarly journals Black pepper-based beverage induced appetite-suppressing effects without altering postprandial glycaemia, gut and thyroid hormones or gastrointestinal well-being: a randomized crossover study in healthy subjects

2018 ◽  
Vol 9 (5) ◽  
pp. 2774-2786 ◽  
Author(s):  
Yoghatama Cindya Zanzer ◽  
Merichel Plaza ◽  
Anestis Dougkas ◽  
Charlotta Turner ◽  
Elin Östman
Keyword(s):  
Glucose Metabolism ◽  
Thyroid Hormones ◽  
Crossover Study ◽  
Healthy Subjects ◽  
Clinical Investigation ◽  
Well Being ◽  
Black Pepper ◽  
Pleiotropic Effects ◽  
Energy Regulation ◽  
Randomized Crossover Study

Pleiotropic effects of spices on health, particularly on glucose metabolism and energy regulation, deserve further clinical investigation into their efficacy.

Effects of hyperglycemia on glucose metabolism before and after oral glucose ingestion in normal men

2006 ◽  
Vol 290 (6) ◽  
pp. E1198-E1204 ◽  
Author(s):  
Vincent Rigalleau ◽  
Marie-Christine Beauvieux ◽  
Jean-Louis Gallis ◽  
Henri Gin ◽  
Phillippe Schneiter ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Glucose Disposal ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Glucose Ingestion ◽  
Before And After ◽  
Endogenous Glucose ◽  
Normal Men

The plasma glucose excursion may influence the metabolic responses after oral glucose ingestion. Although previous studies adressed the effects of hyperglycemia in conditions of hyperinsulinemia, it has not been evaluated whether the route of glucose administration (oral vs. intravenous) plays a role. Our aim was to determine the effects of moderately controlled hyperglycemia on glucose metabolism before and after oral glucose ingestion. Eight normal men underwent two oral glucose clamps at 6 and 10 mmol/l plasma glucose. Glucose turnover and cycling rates were measured by infusion of [2H7]glucose. The oral glucose load was labeled by d-[6,6-2H2]glucose to monitor exogenous glucose appearance, and respiratory exchanges were measured by indirect calorimetry. Sixty percent of the oral glucose load appeared in the systemic circulation during both the 6 and 10 mmol/l plasma glucose tests, although less endogenous glucose appeared during the 10 mmol/l tests before glucose ingestion ( P < 0.05). This inhibitory effect of hyperglycemia was not detectable after oral glucose ingestion, although glucose utilization was increased (+28%, P < 0.05) due to increased nonoxidative glucose disposal [10 vs. 6 mmol/l: +20%, not significant (NS) before oral glucose ingestion; +40%, P < 0.05 after oral glucose ingestion]. Glucose cycling rates were increased by hyperglycemia (+13% before oral glucose ingestion, P < 0.001; +31% after oral glucose ingestion, P < 0.05) and oral glucose ingestion during both the 6 (+10%, P < 0.05) and 10 mmol/l (+26%, P < 0.005) tests. A moderate hyperglycemia inhibits endogenous glucose production and contributes to glucose tolerance by enhancing nonoxidative glucose disposal. Hyperglycemia and oral glucose ingestion both stimulate glucose cycling.

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