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

Maćkowiak, Paweł; Ginalska, E.; Nowak-Strojec, E.; Szkudelski, Tomasz

doi:10.1076/13813455199908107041qft273

Cited by 22 publications

(12 citation statements)

References 36 publications

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“…Thyroid hormone effects on glucose homeostasis and on endocrine function of the pancreas are the result of an interaction of the thyroid hormone with its receptors (Yen 2001). The consequences of hypothyroidism on these metabolic pathways seem to depend on the degree of reduction of circulating thyroid hormones (Mackowiak et al 1999). To date, only a few studies have investigated the effect of thyroid dysfunction and its recovery by thyroid hormone treatment on glucose metabolism, and the results have been controversial (Dessein et al 2004, Stanická et al 2005, Brenta et al 2007, Handisurya et al 2008.…”

Section: Introductionmentioning

confidence: 99%

Impaired insulin secretion from the pancreatic islets of hypothyroidal growth-retarded mice

Taguchi¹,

Tasaki²,

Terakado³

et al. 2010

Journal of Endocrinology

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The growth-retarded (grt) mouse shows thyroid dysfunctionrelated hyporesponsiveness to TSH. Thyroid hormone is a critical regulator of metabolism in many cells; thus, derangement of thyroid function affects many organs and systems. Experiments were conducted focusing on the function of the pancreatic islets in grt mice. We showed occurrence of a fasting hyperglycemia and a decreased plasma insulin level response to a glucose load in grt mice, despite normal insulin molecules being stored in secretory granules of pancreatic islets. We also demonstrated a reduction of insulin secretion in response to glucose administration from islets of grt mice in vitro, while the insulin release in response to KCl stimulation was comparable to that in normal mice, indicating that the isolated islets from grt mice have normal ATPsensitive K C channels and postchannel activity. The mRNA expression levels of glucose transporter 2 and glucokinase in the islets of grt mice were similar to those in normal mice. Triiodothyronine administration to grt mice improved insulin secretion very slightly. On the other hand, mRNA for tyrosylprotein sulfotransferase 2 (Tpst2) was found to be expressed in the pancreatic islets of grt mice. Considering that Tpst2 is the responsible gene of grt mice, mutation of which is associated with a poor function of TSH receptor, the findings raise a possibility of involvement of factors including Tpst2 in the insulin hyposecretion in grt mice.

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Section: Introductionmentioning

confidence: 99%

Impaired insulin secretion from the pancreatic islets of hypothyroidal growth-retarded mice

Taguchi¹,

Tasaki²,

Terakado³

et al. 2010

Journal of Endocrinology

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“…The significance of differences between the means was computed by one way analysis of variance, followed by Multiple Comparison Analysis. Spearman's regression analysis was used to study the significance of correlation among the FT 4 , FT 3 , TSH, HOMA, insulin, glucose and kidney function parameters. P-value less than 0.05 was considered.…”

Section: Discussionmentioning

confidence: 99%

“…They influence these activities by regulating the synthesis and activation of membrane transporter proteins, deiodinase enzymes, and their cellular receptors [2]. Beside their effects on the metabolic pathways, thyroid hormones are also known to regulate insulin secretion and action [3]. However, they may counteract the action of insulin by stimulating the hepatic gluconeogenesis and glycogenolysis and up-regulate the expression of hepatic glucose transporters that accelerate the hepatic glucose output [4].…”

Section: Introductionmentioning

confidence: 99%

The Fasting Serum Insulin and Glucose Levels and the Estimated Insulin Resistance in Clinical and Subclinical Hyperthyroid Patients from Saudi Arabia

Aa¹

2017

Br Biomed Bull

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“…Similar to other studies (9-13), the typical curvilinear Scatchard plots and sigmoidal displacement curves observed during the present investigations and mathematical analysis (not presented) suggest, as is generally observed and accepted (38), that two physiologically different pools of insulin receptors exist: high-affinity (HAIRs) and low-affinity (LAIRs) high capacity receptors. Since liver, muscles and adipose tissue are, as previously shown (10)(11)(12)(13)(14)38), very important targets for insulin, we decided to use C2C12 myocytes and 3T3-L1 preadipocytes. These experimental models have previously been applied (39).…”

Section: Discussionmentioning

confidence: 99%

“…aspects (diet, age, temperature and sickness) of the physiological condition of the organism (11)(12)(13)(14). After binding to the extracellular subunit, the signal is transmitted inside target cells.…”

Section: Evaluation Of Insulin Binding and Signaling Activity Of Newlmentioning

confidence: 99%

Evaluation of insulin binding and signaling activity of newly synthesized chromium(III) complexes in vitro

Nowak¹

2010

Mol Med Rep

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Abstract. In the present study, the influence of chromium(III) complexes (acetate, chloride, glycinate, histidinate, lactate and propionate) on insulin binding and signal transduction [phosphorylation of tyrosine and serine in the insulin receptor substrate (IRS)-1] was investigated in vitro using three experimental models: isolated rat liver membranes and cultured mouse C2C12 myoblasts or 3T3-L1 preadipocytes. The examined complexes did not elevate the binding of insulin to the liver membranes. Moreover, chromium histidinate, lactate, acetate and propionate complexes diminished the specific binding of insulin. Simultaneously, chromium chloride, which did not significantly elevate insulin binding, increased the number of membrane accessible particles of the insulin receptors. However, it was accompanied by slightly diminished affinity of the receptor to the hormone. Chromium acetate and propionate significantly diminished the binding capacity of the low-affinity insulin receptor class. Investigations with the myoblast cell line C2C12 and preadipocyte cell line 3T3-L1 did not allow differentiation of the influence of the examined complexes on insulin binding. Immunodetection of phosphorylated forms of IRS-1 showed that the chromium compounds modulated the transduction of the insulin signal. Chromium glycinate, acetate and propionate decreased the amount of IRS-1 phosphorylated at serine. Since it is generally thought that phosphorylation of serine in IRS-1 may moderate insulin action, the above mentioned chromium complexes may, in this way, enhance insulin effects inside target cells. Phosphorylation of tyrosine in IRS-1, which acts as a stimulatory signal for further steps of insulin action, was elevated after the incubation of 3T3-L1 cells with insulin. Chromium supplementation did not additionally intensify this process. However, in the absence of insulin, chromium glycinate and acetate slightly elevated the level of IRS-1 phosphorylated at tyrosine. This fact may be important in vivo at low levels of insulin in blood. The results indicate that the action of chromium(III) complexes involves a direct effect on the number of receptors accessible to insulin, their affinity to the hormone and the modulation of the signal multiplying proteins by their phosphorylation.

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

Cited by 22 publications

References 36 publications

Impaired insulin secretion from the pancreatic islets of hypothyroidal growth-retarded mice

Impaired insulin secretion from the pancreatic islets of hypothyroidal growth-retarded mice

The Fasting Serum Insulin and Glucose Levels and the Estimated Insulin Resistance in Clinical and Subclinical Hyperthyroid Patients from Saudi Arabia

Evaluation of insulin binding and signaling activity of newly synthesized chromium(III) complexes in vitro

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