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Cited by 38Pancreatic function and diabetesThyroid Disorders and TreatmentsEndoplasmic Reticulum Stress and Disease

Evidence for a deficient pancreatic β-cell response in a rat model of hyperthyroidism

Fukuchi, Mari, Shimabukuro, Michio, Shimajiri, Yoshinori, Oshiro, Yoshito, Higa, Moritake, Akamine, Hiromitsu, Komiya, Ichiro, Takasu, Nobuyuki·2002·Life Sciences
DOI 10.1016/s0024-3205(02)01791-5
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Abstract

To clarify mechanism behind the abnormal glucose tolerance, observed in hyperthyroidism, we studied genomic and nongenomic effects of thyroid hormone on insulin secretion using a rat model of hyperthyroidism. Male Sprague-Dawley rats were intraperitoneally injected with vehicle, low (100 microg/kg) or high dose (600 microg/kg) of thyroxin (T(4)) for 2 weeks. Rats treated with high dose, but not low dose, of T(4), showed an increase in serum T(3) levels, and a decrease in body weight as compared to control rats. In rats treated with either dose of T(4), fasting blood glucose levels were increased, but serum insulin levels were similar to those of controls. After an oral glucose load, blood glucose levels were increased in rats treated with high dose, but not low dose, of T(4). Serum insulin levels after the oral glucose load were decreased in rats treated with either dose of T(4). After an intravenous glucose load, blood glucose levels were comparable among groups, but serum insulin levels tended to be low in T(4)-treated rats. Steady-state blood glucose levels were comparable among groups. The insulin secretory responses to high glucose (20mM) or arginine (10mM) of the isolated pancreas was decreased in rats treated with high dose, but not low dose, of T(4). Mean insulin secretory response to glucose and arginine were decreased by 40.1% and by 60.4% in high-dose-T(4)-treated rats. Addition of T(3) in the perfusion medium decreased glucose-induced insulin release. Ratios of proinsulin mRNA levels to beta-actin mRNA were decreased in the islets of T(4)-treated rats (0.45 +/- 0.07 vs control 0.61 +/- 0.03, p < 0.05). Levels of TR (thyroid hormone nuclear receptor) alpha1 + cErb Aalpha2 mRNA, but not TRbeta1, were decreased in the pancreatic islets of T(4)-treated rats. Calculated islet area was increased, but the number of beta-cells determined immunohistochemically was not increased in T(4)-treated rats, nor the volume density of insulin positive islets. We concluded that a deficient pancreatic beta-cell response to glucose, rather than insulin resistance, was responsible for abnormal glucose tolerance in this model of hyperthyroidism. Thyroid hormone causes a decrease in glucose-induced insulin secretion. We observed nongenomic and genomic effects of thyroid hormone on glucose-induced insulin secretion.

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  • T3 exerts profound effects on the proliferation of pancreatic islet cells and insulin secretion.

    “Moreover, T3 exerts profound effects on the proliferation of pancreatic islet cells and insulin secretion (57, 59).”

    From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [59]

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Authors
Fukuchi, M., Shimabukuro, M., Shimajiri, Y., Oshiro, Y., Higa, M., Akamine, H., Komiya, I., & Takasu, N.
Affiliations
University of the Ryukyus (JP)
Corresponding author
Shimabukuro, Michio
ORCID
Venue
Life Sciences
Publisher
Elsevier BV
Published
2002-07
Volume
71
Issue
9
Pages
1059-1070
ISSN
0024-3205 (ISSN-L)
DOI
10.1016/s0024-3205(02)01791-5
OpenAlex
W2014508254
Cited by
38
References
30
Citations by year
2025: 1 · 2024: 2 · 2023: 3 · 2022: 1 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 1 · 2016: 4 · 2015: 1 · 2014: 2 · 2013: 2
FWCI
1.60
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Life Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
Chinese Academy of Agricultural Sciences
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
Keywords
hyperthyroidism, insulin secretion, pancreatic beta cells, glucose tolerance, thyroxine, triiodothyronine, insulin resistance, glucose-stimulated insulin secretion
MeSH terms
Animals, Base Sequence, Blood Glucose, Disease Models, Animal, Glucose Tolerance Test, Hyperthyroidism, Islets of Langerhans, Male, Thyroid Hormones, Rats, Sprague-Dawley, DNA Primers, Rats

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