Thyroid Hormone Augments GLUT4 Expression and Insulin-Sensitive Glucose Transport System in Differentiating Rat Brown Adipocytes in Culture.

Shimizu, Yasutake; Shimazu, Takashi

doi:10.1292/jvms.64.677

Cited by 21 publications

(12 citation statements)

References 35 publications

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“…Those factors responsible for the high-fat diet induced GLUT4 repression could be arachidonic acids (24,25) or other long chain fatty acids, such as stearic acids, oleic acids, etc (25). Thyroid hormone treatment of rats caused an increase in GLUT4 mRNA and protein level in muscle (26,27) and adipocytes (28).…”

Section: Metabolic and Hormonal Control Of Glut4 In Muscle And Adiposmentioning

confidence: 97%

Regulation of glucose transporter type 4 isoform gene expression in muscle and adipocytes

Kwon

Kim

et al. 2007

IUBMB Life

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SummaryThe gene expression of glucose transporter type 4 isoform (GLUT4) is known to be controlled by metabolic, nutritional, or hormonal status. Understanding the molecular mechanisms governing GLUT4 gene expression is critical, because glucose disposal in the body depends on the activities of GLUT4 in the muscle and adipocytes. The GLUT4 activities are regulated by a variety of mechanisms. One of them is transcriptional regulation. GLUT4 gene expression is regulated by a variety of transcriptional factors in muscle and adipose tissue. These data are accumulating regarding the transcriptional factors regulating GLUT4 gene expression. These include MyoD, MEF2A, GEF, TNF-a, TR-1a, KLF15, SREBP-1c, C/EBP-a, O/E-1, free fatty acids, PAPRg, LXRa, NF-1, etc. These factors are involved in the positive or negative regulation of GLUT4 gene expression. In addition, there is a complex interplay between these factors in transactivating GLUT4 promoter activity. Understanding the mechanisms controlling GLUT4 gene transcription in these tissues will greatly promote the potential therapeutic drug development for obesity and T2DM.

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Section: Metabolic and Hormonal Control Of Glut4 In Muscle And Adiposmentioning

confidence: 97%

Regulation of glucose transporter type 4 isoform gene expression in muscle and adipocytes

Kwon

Kim

et al. 2007

IUBMB Life

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“…We demonstrated that T 3 replacement can completely recover the impaired glucose tolerance in grt mice, and that the plasma levels of insulin in response to a glucose load were only slightly increased in T 3 -treated grt mice, indicating that hypothyroidism is associated with a deterioration of glucose metabolism. The recovery of impaired blood glucose levels in T 3 -treated grt mice may be associated with increased GLUT4 localized in the myocytes and adipocytes that is involved in glucose transport, since GLUT4 protein expression is regulated by T 3 (Shimizu & Shimazu 2002). It has been reported that although subjects with hypothyroidism are characterized by attenuated plasma insulin concentrations and increased glucagon concentrations in the basal state, T 4 replacement can, among other effects, result in partial amelioration of insulin secretion and improved insulin sensitivity (Handisurya et al 2008).…”

Section: Tpst2mentioning

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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“…Increase in both hepatic insulin resistance (11,12) and insulin-mediated glucose uptake is observed in hyperthyroidism as compared with euthyroid conditions (11). Thyroid hormones influence insulin action in skeletal muscle and adipose tissue in part by upregulating the expression of the muscle/fat-specific glucose transporter 4 (13,14). In contrast, studies in hypothyroid conditions show a decrease in both hepatic insulin resistance (12) and insulin-mediated glucose uptake in muscles (10,12).…”

Section: Introductionmentioning

confidence: 99%

Association Analyses of Variants in the DIO2 Gene with Early-Onset Type 2 Diabetes Mellitus in Pima Indians

Nair

Muller

Ortega

et al. 2012

Thyroid

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Background: The type 2 deiodinase gene (DIO2) encodes a deiodinase that converts the thyroid prohormone, thyroxine, to the biologically active triiodothyronine. Thyroid hormones regulate energy balance and may also influence glucose metabolism. Therefore, we hypothesized that variations in DIO2 could contribute to obesity or type 2 diabetes mellitus (T2DM) in Pima Indians. Methods: Sequencing of the DIO2 gene in DNA from 83 Pima Indians identified 12 single-nucleotide polymorphisms (SNPs). Several of these SNPs were in perfect genotypic concordance among the 83 samples that were sequenced, and all 12 could be divided into five linkage disequilibrium groups. One representative SNP from each group (Thr92Ala, rs225011, rs225015, rs6574549, and a rare 5¢ flanking SNP) was selected for further genotyping for association analyses. In this study, the five selected variants in DIO2, as described above, were genotyped in three groups of Pima Indians: (i) a case (n = 150)/control (n = 150) group for early-onset T2DM (onset age < 25 years); (ii) a case (n = 362)/control (n = 127) group for obesity; (iii) a large (n = 1,311, cases n = 810/ controls n = 501) family-based group, of which 256 nondiabetic subjects had undergone detailed metabolic phenotyping. Results: The Thr92Ala variant common in Pima Indians, rs225011, and rs225015 were modestly associated with early-onset T2DM ( p = 0.01-0.04) in the case-control study, but were not associated with obesity in the obesity case-control study, nor associated with T2DM (at any age) or body-mass index (BMI; as a quantitative trait) in the family-based analysis. Thr92Ala, rs225011, rs225015, and rs6574549 were also nominally associated with hepatic glucose output ( p = 0.02). rs6574549 was associated with fasting insulin ( p = 0.02), insulin action ( p = 0.04), and energy expenditure ( p = 0.02). None of these nominal associations remained statistically significant after corrections for multiple testing. Conclusions: We propose that variation in DIO2 may have a subtle role in altering metabolic processes that lead to early-onset T2DM, but this gene does not have a large impact on T2DM at older ages, nor does DIO2 influence BMI in the Pima Indian population.

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Thyroid Hormone Augments GLUT4 Expression and Insulin-Sensitive Glucose Transport System in Differentiating Rat Brown Adipocytes in Culture.

Cited by 21 publications

References 35 publications

Regulation of glucose transporter type 4 isoform gene expression in muscle and adipocytes

Regulation of glucose transporter type 4 isoform gene expression in muscle and adipocytes

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

Association Analyses of Variants in the DIO2 Gene with Early-Onset Type 2 Diabetes Mellitus in Pima Indians

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