Impaired glucose‐stimulated insulin secretion and reduced β‐cell mass in pancreatic islets of hyperthyroid rats

Karbalaei, Narges; Noorafshan, Ali; Hoshmandi, Ebrahim

doi:10.1113/ep085627

Cited by 20 publications

(10 citation statements)

References 41 publications

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“…Treatment with high levels of T4 could induce pancreatic β cell apoptosis, as was shown by an increase in transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) and caspase-3 expressions in rat β cells [ 89 ]. Recently, it was demonstrated that impaired glucose-stimulated insulin secretion and reduced β cell mass occurred in pancreatic islets of hyperthyroid rats [ 90 ]. The former effect may be related to decreased sensitivity of ATP-sensitive K + (K + (ATP)) and L-type Ca 2+ channels of the β cells.…”

Section: Roles Of Thyroid and Thyroid Hormone In Pancreas Pathogenmentioning

confidence: 99%

The Roles of Thyroid and Thyroid Hormone in Pancreas: Physiology and Pathology

Chen

Xie

Shen

et al. 2018

International Journal of Endocrinology

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It is widely accepted that thyroid hormones (THs), secreted from the thyroid, play important roles in energy metabolism. It is also known that THs also alter the functioning of other endocrine glands; however, their effects on pancreatic function have not yet been reviewed. One of the main functions of the pancreas is insulin secretion, which is altered in diabetes. Diabetes, therefore, could be related to thyroid dysfunction. Earlier research on this subject focused on TH regulation of pancreas function (such as insulin secretion) or on insulin function through TH-mediated increase of energy metabolism. Afterwards, epidemiological investigations and animal test research found a link between autoimmune diseases, thyroid dysfunction, and pancreas pathology; however, the underlying mechanisms remain unknown. Furthermore, recent studies have shown that THs also play important roles in pancreas development and on islet pathology, both in diabetes and in pancreatic cancer. Therefore, an overview of the effects of thyroid and THs on pancreas physiology and pathology is presented. The topics contained in this review include a summary of the relationship between autoimmune thyroid dysfunction and autoimmune pancreas lesions and the effects of THs on pancreas development and pancreas pathology (diabetes and pancreatic cancer).

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Section: Roles Of Thyroid and Thyroid Hormone In Pancreas Pathogenmentioning

confidence: 99%

The Roles of Thyroid and Thyroid Hormone in Pancreas: Physiology and Pathology

Chen

Xie

Shen

et al. 2018

International Journal of Endocrinology

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“…A reduced volume of pancreatic islets and a lower number of insulin-positive cells have been demonstrated in rats with experimentally induced hyperthyroidism. A defective insulin secretory response due to a possible defect in K ATP and L-type calcium channels was also noted [25]. Similarly, severe hyperthyroidism has also been shown to induce apoptosis of beta cells and to accelerate the rate of apoptosis of pancreatic ductal cells, which serve as precursors of beta cells.…”

Section: Discussionmentioning

confidence: 99%

Insulin Sensitivity and Beta-Cell Function in Graves’ Disease and Their Changes with the Carbimazole-Induced Euthyroid State

et al. 2019

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Background and Objective: Thyroid hormones play an important role in intermediate metabolism, and abnormal glucose tolerance is often observed in patients with hyperthyroidism. Several pathogenic mechanisms have been proposed as contributors. However, there is no conclusive evidence in the existing literature regarding the predominant underlying pathophysiology. Our objective was to determine the changes in insulin resistance parameters and beta-cell function in patients with Graves’ disease following restoration of a euthyroid state. Methodology: This was an observational study with a before-after study design. Forty-five treatment-naïve adults with Graves’ diseases were included and 36 completed the study. An oral glucose tolerance test was performed at baseline and after 3 months of achieving a stable euthyroid state to assess glucose tolerance, insulin sensitivity, and beta-cell function. All patients were treated with antithyroid medication. The outcome measures studied were the Homeostasis Model Assessment-2 Insulin Resistance (HOMA2-IR), Matsuda index, and Insulin Secretion-Sensitivity Index (ISSI)-2. Results: Two-thirds of the patients had abnormal glucose tolerance at baseline. Among those with abnormal glucose tolerance at baseline, 34.7% had persistent abnormality during follow-up. During follow-up, no significant change was noted in the indices of insulin resistance. Patients with abnormal glucose tolerance had a significantly lower ISSI-2 index at baseline and it improved after achieving a euthyroid state. Conclusions: Abnormal glucose tolerance is a significant metabolic consequence in patients with Graves’ disease. Decreased beta-cell function was observed among those with abnormal glucose tolerance and it improved during follow-up. In a proportion of patients, abnormal glucose tolerance persisted after 3 months, emphasizing the need for continued follow-up.

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“…Moreover, the role of TH has been demonstrated particularly in glucose homeostasis [ 43 ]. Indeed, hyperthyroid rats showed reduced glucose tolerance and reduced insulin-secretory capacity of β cells, in addition to an increased hepatic insulin resistance [ 44 ]. Similarly, hypothyroidism promotes glucose intolerance in hypothyroid non-diabetic mice [ 45 ].…”

Section: Effects Of Th On Central Metabolismmentioning

confidence: 99%

Integrating Thyroid Hormone Signaling in Hypothalamic Control of Metabolism: Crosstalk Between Nuclear Receptors

Kouidhi

Clerget-Froidevaux

2018

IJMS

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The obesity epidemic is well recognized as a significant global health issue. A better understanding of the energy homeostasis mechanisms could help to identify promising anti-obesity therapeutic strategies. It is well established that the hypothalamus plays a pivotal role governing energy balance. The hypothalamus consists of tightly interconnected and specialized neurons that permit the sensing and integration of several peripheral inputs, including metabolic and hormonal signals for an appropriate physiological response. Current evidence shows that thyroid hormones (THs) constitute one of the key endocrine factors governing the regulation and the integration of metabolic homeostasis at the hypothalamic level. THs modulate numerous genes involved in the central control of metabolism, as TRH (Thyrotropin-Releasing Hormone) and MC4R (Melanocortin 4 Receptor). THs act through their interaction with thyroid hormone receptors (TRs). Interestingly, TH signaling, especially regarding metabolic regulations, involves TRs crosstalk with other metabolically linked nuclear receptors (NRs) including PPAR (Peroxisome proliferator-activated receptor) and LXR (Liver X receptor). In this review, we will summarize current knowledge on the important role of THs integration of metabolic pathways in the central regulation of metabolism. Particularly, we will shed light on the crosstalk between TRs and other NRs in controlling energy homeostasis. This could be an important track for the development of attractive therapeutic compounds.

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Impaired glucose‐stimulated insulin secretion and reduced β‐cell mass in pancreatic islets of hyperthyroid rats

Cited by 20 publications

References 41 publications

The Roles of Thyroid and Thyroid Hormone in Pancreas: Physiology and Pathology

The Roles of Thyroid and Thyroid Hormone in Pancreas: Physiology and Pathology

Insulin Sensitivity and Beta-Cell Function in Graves’ Disease and Their Changes with the Carbimazole-Induced Euthyroid State

Integrating Thyroid Hormone Signaling in Hypothalamic Control of Metabolism: Crosstalk Between Nuclear Receptors

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