Glucoregulatory Function of Thyroid Hormones: Interaction with Insulin Depends on the Prevailing Glucose Concentration*

Müller, Manfred J.; Schütz, Burkhard; Huhnt, H.J.; Zick, R.; Mitzkat, H. J.; Mühlen, A. von zur

doi:10.1210/jcem-63-1-62

Cited by 34 publications

(21 citation statements)

References 33 publications

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“…Since the response of (or to) catecholamines may differ between the thyroid states, this might contribute to our results. In fact, the glycaemic response to epinephrine infusion was also reduced by hyperthyroidism [lo, 191. It should be mentioned that our data in moderate hyperthyroid miniature pigs differ from results obtained in thyrotoxic subjects, where hepatic and/or peripheral insulin resistance is frequently observed [24-261. Since an increased insulin sensitivity is also observed in moderately hyperthyroid man [4], the different results are most probably explained by the degree of hyperthyroidism, and are obviously not due to species specific effects of thyroid hormones. This leads us to the more general idea that near physiological effects of T3 differ from its pharmacological actions.…”

Section: Discussionmentioning

confidence: 92%

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Glucoregulatory function of glucagon in hypo-, eu- and hyperthyroid miniature pigs

et al. 1988

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The glucoregulatory function of glucagon was investigated in hypo-, eu- and hyperthyroid miniature pigs. Infusion glucagon, (3 ng x kg body weight-1.min-1) transiently increased blood glucose (p less than 0.01) and hepatic glucose production (p less than 0.01) in euthyroidism, but was without effect in hyperthyroidism. Infusing glucagon plus somatostatin (2 ng x kg body weight-1.min-1 and 0.2 microgram x kg body weight-1.min-1) transiently increased blood glucose (delta 3.0 to 4.3 mmol/l) and hepatic glucose production (delta 3.3 to 7.7 mumol x kg body weight-1.min-1) in all thyroid states, the effect was less pronounced in hyperthyroid pigs. By contrast, hypoglucagonaemia (74 to 107 pg/ml) at basal insulin (28 to 35 microU/ml) provoked hypoglycaemia (1.4 to 2.2 mmol/l) and a fall in glucose production (delta 4.7 to 8.3 mumol x kg body weight-1.min-1), which was independent of the thyroid state; the effect was most pronounced in hyperthyroidism (p less than 0.01). Hepatic glycogen content, arterial gluconeogenic precursor concentrations as well as the glycaemic response (delta 0.60 mmol/l) to alanine infusion (23 mumol x kg body weight-1.min-1) were all unaffected by hyperthyroidism. We conclude that moderate experimental hyperthyroidism reduces glucagon action due to reduced glycogen mobilisation. This may in part result from increased insulin sensitivity.

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Section: Discussionmentioning

confidence: 92%

“…With respect to insulin we could show recently that moderate hyperthyroidism may increase hepatic as well as peripheral insulin sensitivity [3,4]. With respect to glucagon, its portal and peripheral levels are frequently elevated in clinical as well as experimental hyperthyroidism [5,6].…”

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confidence: 99%

Glucoregulatory function of glucagon in hypo-, eu- and hyperthyroid miniature pigs

et al. 1988

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“…32,33 Steady-state glucose disposal rate was calculated from the mean rate of exogenous glucose infusion during the last 30 min of the clamp, after glucose space correction (M-value (mg kg À1 min À1 )). Steady-state concentrations of serum insulin and plasma glucose (coefficient of variation (CV) 6.0 ± 3.1%) were assayed using the previously described methods.…”

Section: Hyperinsulinemic Euglycemic Clampmentioning

confidence: 99%

Effects of brief perturbations in energy balance on indices of glucose homeostasis in healthy lean men

et al. 2011

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BACKGROUND:Little is known about the effects of short-term caloric restriction (CR) and overfeeding (OF) on glucose homeostasis in healthy lean individuals. In addition, it remains unclear whether the effects of CR and OF are reversed by a complementary feeding period. METHODS: Ten healthy men participated in two cycles of controlled 7-day periods of CR and refeeding (RF; protocol A), and OF and CR (protocol B) at ±60% energy requirement. At baseline, insulin sensitivity (IS) was assessed by euglycemic clamp (M). Before and during each feeding cycle, fasting and oral glucose tolerance test-derived indices were used to estimate glucose tolerance, IS and glucose-stimulated insulin secretion. RESULTS: Clamp tests revealed normal IS at baseline (M-values 9.4 ± 2.1 mg kg À1 min À1 , coefficient of variation (CV) inter 22%). M-values were significantly correlated with indices of IS. In protocol A, CR-induced weight loss (À3.0±0.4 kg) was associated with an increase in fasting IS. Postprandial IS and glucose-stimulated insulin secretion remained unchanged, but glucose tolerance decreased. RF decreased fasting and postprandial IS at increased glucose-stimulated insulin secretion. In protocol B, OF significantly increased the body weight ( þ 1.6±0.9 kg). Concomitantly, fasting and postprandial IS decreased at increased glucose-stimulated insulin secretion. Subsequent CR reversed these effects. Inter-individual variability in indices of glucose metabolism was high with coefficients of variation ranging from 9 to 59%. CONCLUSION: Significant changes in glucose metabolism are evident within 7-day periods of controlled OF and underfeeding. Although IS was impaired at the end of the CR --RF cycle, IS was normalized after the OF --CR cycle. At different feeding regimens, homeostatic responses of glucose metabolism were highly variable. Keywords: insulin secretion; insulin sensitivity; glucose homeostasis; weight gain; energy balance INTRODUCTION Long-term perturbations in energy balance, either by overfeeding (OF) or underfeeding, are known to modulate insulin sensitivity (IS). Chronic OF and obesity are commonly characterized by insulin resistance, 1 which has been shown to be completely 2 or partially reversed by acute caloric restriction (CR), as well as by moderate weight loss. 3 --5 On the other hand, IS is preserved or even improved with chronic CR in patients with anorexia nervosa and returned to normal values at the end of refeeding (RF). 6 Although considerable research has been devoted to individuals outside the normal range of body weight, there are only few studies examining the effects of short-term controlled perturbations in energy balance on IS in lean subjects without confounding metabolic abnormalities. 7 --17 Moreover, these studies provide discordant findings that may depend on duration and degree of energy imbalance and macronutrient composition of the diets. Fasting (1 --3 days) consistently caused a decline in IS assessed by clamp-and intravenous glucose tolerance test. 7,8,17 Studies with less severe ...

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“…Moreover, using the regular euglycaemic hyperinsulinaemic clamp, it was demonstrated that there is an impairment in the insulin-induced suppression of glucose production in hyperthyroid patients [2,8]. At low insulin levels, insulinstimulated glucose disposal is usually unaffected [2,[8][9][10][11], whereas it has been reported to be decreased [2], unchanged [8,10,12,13] or even increased [9,11,14,15] at high insulin levels. Other researchers reported that thyroid hormones blunted the insulin-induced increases in the total distribution volume of the exchanging pool of glucose, possibly reflecting an acceleration of intracellular glucose degradation [10].…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, the actions of thyroid hormones are strongly dose-dependent. In addition, the interaction with insulin action depends on the prevailing glucose concentration [9]. All studies have been performed in patients with clinical thyrotoxicosis and in thyroid hormone-treated healthy volunteers.…”

Section: Introductionmentioning

confidence: 99%

Response of glucose disposal to hyperinsulinaemia in human hypothyroidism and hyperthyroidism

Rochon

Tauveron²,

Dejax

et al. 2002

Clinical Science

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We have examined insulin action on glucose metabolism in six hypothyroid patients before and after regular thyroid hormone treatment, and in six healthy volunteers before and after transient induction of moderate hyperthyroidism. Insulin was infused under euglycaemic and eukalaemic clamps. An appropriate amino acid infusion was used to blunt insulin-induced decreases in amino acid levels. Glucose kinetics were assessed using a primed continuous infusion of [6,6-(2)H(2)]glucose. The results showed that basal plasma insulin and glucose levels (i.e. before infusion) were similar in each case. Despite similar insulin infusion rates, the plateau value of insulin was lower after thyroid treatment in both hypothyroid patients and healthy volunteers. The rate of exogenous glucose needed to maintain plasma glucose at a steady-state level was increased by thyroid hormone in hypothyroid patients (P <0.05), but not in healthy volunteers. Thyroid treatment resulted in a significant increase in basal glucose disposal in both groups (P <0.05). Insulin, in conjunction with glucose and amino acids, significantly stimulated glucose disposal (P <0.05) under all conditions. The incremental increase in glucose disposal after infusion tended to be higher following thyroid hormone treatment, but this was not statistically significant. However, the ratio of the incremental increase in glucose disposal to the increase in plasma insulin was significantly improved after thyroid hormone treatment in hypothyroid patients (P <0.05). It was also increased in healthy volunteers, but not significantly. We conclude that thyroid hormones improve the ability of insulin to stimulate glucose disposal related to insulinaemia. This phenomenon may be highly sensitive, because it was only apparent at low thyroid hormone levels.

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Glucoregulatory Function of Thyroid Hormones: Interaction with Insulin Depends on the Prevailing Glucose Concentration*

Cited by 34 publications

References 33 publications

Glucoregulatory function of glucagon in hypo-, eu- and hyperthyroid miniature pigs

Glucoregulatory function of glucagon in hypo-, eu- and hyperthyroid miniature pigs

Effects of brief perturbations in energy balance on indices of glucose homeostasis in healthy lean men

Response of glucose disposal to hyperinsulinaemia in human hypothyroidism and hyperthyroidism

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