Effect of short- and long-term experimental hyperthyroidism on plasma glucose level and insulin secretion during an intravenous glucose load and on insulin binding, insulin receptor kinase activity, and insulin action in adipose tissue

Casla, A.; Arrieta, Francisco; Grant, Carlos; Casanova, Benito; Rovira, Adela

doi:10.1016/0026-0495(93)90052-p

Cited by 11 publications

(12 citation statements)

References 47 publications

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“…Previous results obtained in isolated adipocytes (Casla et al 1993, Matthaei et al 1995 and in isolated skeletal muscles (Weinstein et al 1994) from hyperthyroid rats have reported that T 3 produced an increase in the insulinstimulated glucose transport in 3T3-L1 adipocytes. In our study, insulin sensitivity was enhanced by T 3 treatment.…”

Section: Discussionmentioning

confidence: 87%

“…Thyroid hormone has been shown to increase glucose disposal in humans and in animals (Hardeveld & Kassenaar 1977, Sandler et al 1983, Foss et al 1990, Casla et al 1993 and to stimulate glucose transport in cultured cells (Segal & Gordon 1977). The cellular glucose uptake by facilitated diffusion is mediated by a family of homologous glucose transporter proteins, of which the insulinresponsive glucose transporter (GLUT4) is expressed primarily in adipose tissue and skeletal and cardiac muscle, and the GLUT1 glucose transporter is expressed in several tissues as well as in cultured cell lines.…”

Section: Introductionmentioning

confidence: 99%

“…The stimulatory effect of thyroid hormone on glucose uptake has been related to an increase in glucose transporter proteins (Casla et al 1993). The excess of thyroid hormone affects the two glucose carrier isoforms, GLUT1 and GLUT4, in a different way depending on specific tissues.…”

Section: Introductionmentioning

confidence: 99%

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Stimulation of glucose transport by thyroid hormone in 3T3-L1 adipocytes: increased abundance of GLUT1 and GLUT4 glucose transporter proteins

Romero¹,

Casanova²,

Pulido³

et al. 2000

Journal of Endocrinology

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In 3T3-L1 adipocytes we have examined the effect of tri-iodothyronine (T 3 ) on glucose transport, total protein content and subcellular distribution of GLUT1 and GLUT4 glucose transporters. Cells incubated in T 3 -depleted serum were used as controls. Cells treated with T 3 (50 nM) for three days had a 3·6-fold increase in glucose uptake (P<0·05), and also presented a higher insulin sensitivity, without changes in insulin binding. The two glucose carriers, GLUT1 and GLUT4, increased by 87% (P<0·05) and 90% (P<0·05), respectively, in cells treated with T 3 . Under non-insulin-stimulated conditions, plasma membrane fractions obtained from cells exposed to T 3 were enriched with both GLUT1 (3·29 0·69 vs 1·20 0·29 arbitrary units (A.U.)/5 µg protein, P<0·05) and GLUT4 (3·50 1·16 vs 0·82 0·28 A.U./5 µg protein, P<0·03). The incubation of cells with insulin produced the translocation of both glucose transporters to plasma membranes, and again cells treated with T 3 presented a higher amount of GLUT1 and GLUT4 in the plasma membrane fractions (P<0·05 and P<0·03 respectively). These data indicate that T 3 has a direct stimulatory effect on glucose transport in 3T3-L1 adipocytes due to an increase in GLUT1 and GLUT4, and by favouring their partitioning to plasma membranes. The effect of T 3 on glucose uptake induced by insulin can also be explained by the high expression of both glucose transporters.

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Section: Discussionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

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Stimulation of glucose transport by thyroid hormone in 3T3-L1 adipocytes: increased abundance of GLUT1 and GLUT4 glucose transporter proteins

Romero¹,

Casanova²,

Pulido³

et al. 2000

Journal of Endocrinology

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“…However, opinions on the influence of thyrotoxicosis on insulin secretion vary. Taylor et al (1985) stated in thyrotoxic humans normal insulin secretion, whereas Casla et al (1993) found both slightly decreased level of insulin after 10 days treatment of rats with T 4 and its doubled concentration after 30 days. Our results are in a good agreement with many authors who stated that the insulin secretion increases after the administration of thyroid hormones (Okajima & Ui, 1978;Heise et al, 1982;Lenzen & Bailey, 1984;Diaz et al, 1993;Fickova et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…These alterations may result from disturbances in insulin reception by target tissues. Both stimulatory (Heise et al 1982;Casla et al 1993) and inhibitory (Taylor et al 1985;Fickova et al 1997) effects of T 4 on insulin binding were found.…”

Section: Introductionmentioning

confidence: 90%

The Influence of Hypo- and Hyperthyreosis on Insulin Receptors and Metabolism

Maćkowiak¹,

Ginalska²,

Nowak-Strojec³

et al. 1999

Archives of Physiology and Biochemistry

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Changes in thyroid status affect metabolism not only directly, but influence it also by alterations in insulin secretion and action. Despite several investigations, these effects are, however, poorly characterised or even controversial. The aim of the studies was to investigate the effect of hyperthyreosis (HT) and hypothyreosis (HPT) on insulin binding by rat liver membranes. Some metabolic parameters reflecting insulin and thyroid hormones action were also determined. HT and HPT were developed by daily administration for 3 weeks of thyroxine (T (4) ) and thiouracil (TU), respectively. Experimental hyperthyreosis and hypothyreosis caused deep changes in metabolism. The greatest alterations were observed in body and thyroid glands weight, blood triiodothyronine (T (3) ), T (4), glucose, and insulin levels, liver glycogen amount and number of insulin receptors. HT reflected in rats in slower rate of growth and in smaller thyroid glands weight. In comparison to controls, T (4) concentration in HT was almost doubled and it was reduced by about 30% in HPT. Also, T(3), insulin and glucose levels in HT were heightened. Simultaneously, binding of insulin to liver membranes was elevated in HT and reduced in HPT. In HT the number of high affinity insulin receptors (HAIRs) and low affinity insulin receptors (LAIRs) was increased, whereas in HPT the amount of HAIRs was diminished. HT caused a drastic reduction of glycogen concentration in liver, but no changes were observed for muscle glycogen. Considering lipid metabolism, only free fatty acids (FFA) level in blood was changed (in HPT), but no differences were observed in serum concentration of triglycerides and cholesterol. Several metabolic changes observed in HT and HPT seem to be the dire ct consequence of alterations of thyroid hormone concentrations. These disturbances, together with the direct effect of HT or HPT on insulin secretion, binding and action lead, in turn, to changes in the other metabolic parameters. As a result of these disturbances the adaptive mechanisms appear. One of them is change in the number of insulin membrane receptors taking place even against the well known "down-regulation" theory.

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Pyrroloquinoline quinone ameliorates l‐thyroxine‐induced hyperthyroidism and associated problems in rats

Kumar¹,

Kar²,

Panda³

2014

Cell Biochemistry & Function

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Pyrroloquinoline quinone (PQQ) is believed to be a strong antioxidant. In this study, we have evaluated its hitherto unknown role in l-thyroxin (L-T4 )-induced hyperthyroidism considering laboratory rat as a model. Alterations in the serum concentration of thyroxin (T4 ) and triiodothyronine (T3 ); lipid peroxidation (LPO) of liver, kidney, heart, muscles and brain; in the endogenous antioxidants such as superoxide dismutase, catalase and glutathione and in serum total cholesterol, high-density lipoprotien, triglycerides, serum glutamate pyruvate transaminase (SGPT), serum glutamate oxaloacetate transaminase (SGOT) and urea were evaluated. Administration of l-T4 (500-µg kg(-1) body weight) enhanced not only the serum T3 and T4 levels but also the tissue LPO, serum SGOT, SGPT and urea with a parallel decrease in the levels of antioxidants and serum lipids. However, on simultaneous administration of PQQ (5 mg kg(-1) for 6 days), all these adverse effects were ameliorated, indicating the potential of PQQ in the amelioration of hyperthyroidism and associated problems. Possibly, the curative effects were mediated through inhibition of oxidative stress. We suggest that PQQ may be considered for therapeutic use for hyperthyroidism after dose standardization.

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Effect of short- and long-term experimental hyperthyroidism on plasma glucose level and insulin secretion during an intravenous glucose load and on insulin binding, insulin receptor kinase activity, and insulin action in adipose tissue

Cited by 11 publications

References 47 publications

Stimulation of glucose transport by thyroid hormone in 3T3-L1 adipocytes: increased abundance of GLUT1 and GLUT4 glucose transporter proteins

Stimulation of glucose transport by thyroid hormone in 3T3-L1 adipocytes: increased abundance of GLUT1 and GLUT4 glucose transporter proteins

The Influence of Hypo- and Hyperthyreosis on Insulin Receptors and Metabolism

Pyrroloquinoline quinone ameliorates l‐thyroxine‐induced hyperthyroidism and associated problems in rats

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