Glucose transporter 2 concentrations in hyper- and hypothyroid rat livers

Mokuno, T; Uchimura, Keiko; Hayashi, Rina; Hayakawa, Naokazu; Miyamoto, Masaki; Nagata, Mutsuko; Kakizawa, Hideaki; Sawai, Yusuke; Kotake, Motoko; Oda, Naohisa; Nakai, Asami; Nagasaka, Akio; Itoh, Mitsuyasu

doi:10.1677/joe.0.1600285

Cited by 45 publications

(27 citation statements)

References 15 publications

(1 reference statement)

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“…Stimulation of the glycolysis system in the presence of thyroid hormone excess can lead to excess lactic acid, a precursor to gluconeogenesis, which enters the Cori cycle to stimulate gluconeogenesis [4]. Furthermore, thyroid hormones increase the cell membrane level of GLUT2, a major glucose transporter isoform expressed in hepatocytes [11,12], resulting in increased release of glucose into the blood from the liver, which serves as a cause of abnormal glucose metabolism. In the presence of thyrotoxicosis, catecholamine stimulation leads to enhanced lipid degradation, thereby increasing free fatty acids, which in turn stimulates gluconeogenesis in the liver [13,14].…”

Section: Figmentioning

confidence: 99%

Glucose variability before and after treatment of a patient with Graves’ disease complicated by diabetes mellitus: Assessment by continuous glucose monitoring

et al. 2014

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HypertHyroidism can interfere with glucose metabolism through various mechanisms, and 50% of patients with thyrotoxicosis are reported to have abnormal glucose tolerance [1]. Known factors responsible for abnormal glucose tolerance include enhanced glucose absorption via the digestive tract [2, 3] and increased endogenous gluconeogenesis [4]. However, as a compensatory mechanism, excessive insulin secretion [5,6] is typically effective; hyperglycemia is often absent even in patients with thyrotoxicosis.The prevalent use of continuous glucose monitoring (CGM) has provided details on blood glucose vari- Abstract. A 48-year-old woman was diagnosed and treated for Graves' disease (GD) in 1999 but she discontinued treatment at her own discretion. In 2011, she was admitted to a local hospital for management of thyrotoxic crisis. Treatment with propylthiouracil, iodide potassium (KI), and prednisolone (PSL) was started, which resulted in improvement of the general condition. PSL and KI were discontinued before she was transferred to our hospital. At the local hospital, fasting plasma glucose (FPG) was 212 mg/dL and hemoglobin A1c concentration was 11.2%; intensive insulin therapy had been instituted. Upon admission to our hospital, FPG level was 122 mg/dL, but insulin secretion was compromised, suggesting aggravation of thyroid function and deterioration of glycemic control. The FPG level increased to 173 mg/dL; continuous glucose monitoring (CGM) identified dawn phenomenon at approximately 0400 h. Resumption of KI resulted in improvement of FPG and disappearance of the dawn phenomenon, as assessed by CGM. These results indicate that in patients with compromised insulin secretion, hyperthyroidism can induce elevation of not only postprandial blood glucose, but also FPG level due to the dawn phenomenon and that the dawn phenomenon can be alleviated with improvement in thyroid function. To our knowledge, no studies have assessed glucose variability by CGM before and after treatment of Graves' disease. The observations made in this case shed light on the understanding of abnormal glucose metabolism associated with Graves' disease.Key words: Graves' disease (GD), Continuous glucose monitoring (CGM), Dawn phenomenon ability patterns that were otherwise not possible with the self-monitoring of blood glucose (SMBG). To our knowledge, however, no studies have assessed glucose variability by CGM before and after treatment of hyperthyroidism. Here, we report a patient with Graves' disease complicated by diabetes mellitus, who presented with disturbance of endogenous insulin secretion. In this patient, hyperthyroidism resulted in not only postprandial hyperglycemia but also elevation of fasting plasma glucose (FPG) level due to the dawn phenomenon, and CGM was employed to confirm alleviation of the dawn phenomenon following improvement of thyroid function. research design and methodsThe CGM device used to assess intraday glucose variability in the presence of hyperthyroidism (CGMS ® System Gold™, Medtronic, Minneapolis, MN) can ...

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Section: Figmentioning

confidence: 99%

Glucose variability before and after treatment of a patient with Graves’ disease complicated by diabetes mellitus: Assessment by continuous glucose monitoring

et al. 2014

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“…For example, T 3 can modulate the mRNA and protein levels of these molecules in pancreatic islets (García-Flores et al 2001). In addition, thyroid hormones regulate hepatic glucose transport by altering the expression of Glut2 mRNA and protein levels in hepatocytes (Weinstein et al 1994, Kemp et al 1997, Mokuno et al 1999. Thyroid hormone is also involved in the regulation of Gk gene transcription in liver (Höppner & Seitz 1989).…”

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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“…First: Hyperthyroid patients have been shown to have increased circulating pro-insulin than active insulin levels and had reduced C-peptide levels compared to their euthyroid counterparts, suggesting an underlying defect in the proinsulin processing [18]. Second: The hyperthyroid patients are believed to have enhanced intestinal glucose absorption due to the increased expression of intestinal membrane glucose transporters [22,23]. Third: Increased rate of gluconeogenesis and hepatic glucose output by the expression of the hepatocyte membrane GluT 2 [24].…”

Section: Discussionmentioning

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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Glucose transporter 2 concentrations in hyper- and hypothyroid rat livers

Cited by 45 publications

References 15 publications

Glucose variability before and after treatment of a patient with Graves’ disease complicated by diabetes mellitus: Assessment by continuous glucose monitoring

Glucose variability before and after treatment of a patient with Graves’ disease complicated by diabetes mellitus: Assessment by continuous glucose monitoring

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

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