Impaired thyrotrophin secretion following the administration of thyrotrophin-releasing hormone in type II diabetes mellitus

Small, M.; Cohen, Helen; MacLean, J.; Beastall, G. H.; MacCuish, A C

doi:10.1136/pgmj.62.728.445

Cited by 7 publications

(4 citation statements)

References 14 publications

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“…TSH secretion may be suppressed, and the response to TRH flat, in some patients with diabetes mellitus (Kabadi, 1984;Small et al, 1986;Schnack & Schernthaner, 1987). In this study, patients with Cushing's syndrome and diabetes had slightly (but not significantly) lower basal and stimulated TSH levels, and they had significantly more often a 'flat' TSH response to TRH.…”

Section: Discussionmentioning

confidence: 51%

Tsh Secretion In Cushing's Syndrome: Relation To Glucocorticoid Excess, Diabetes, Goitre, And The ‘Sick Euthyroid Syndrome’

Benker¹,

Raida²,

Olbricht³

et al. 1990

Clinical Endocrinology

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Thyrotrophin (TSH) secretion was studied in 63 patients with Cushing's syndrome (53 patients with pituitary dependent Cushing's disease, eight with adrenocortical tumours, and two with the ectopic ACTH syndrome). Prior to treatment, TSH response to 200 micrograms of TRH intravenously was significantly decreased compared to controls; TSH response was 'flat' (increment less than 2 mU/l) in 34 patients (54%). Patients with a flat response to TRH had significantly higher morning and midnight cortisol levels than patients with a TSH response of 2 mU/l and more; this was not due to differences in serum thyroid hormone levels. Basal TSH, TSH increment after TRH, and stimulated TSH value, but not serum triiodothyronine, were correlated with cortisol measurements (0800 h serum cortisol, midnight cortisol, and urinary free corticoid excretion). After exclusion of 40 patients with additional disease (severe systemic disease, diabetes mellitus, or goitre), cortisol-TSH correlations were even more pronounced (r = -0.73 for midnight cortisol and stimulated TSH levels), while in the patients with additional complications, these correlations were slight or absent. Successful treatment in 20 patients was associated with a rise in thyroid hormone levels and the TSH response to TRH. These results indicate that (1) the corticoid excess but not serum T3 is the principal factor regulating TSH secretion in Cushing's syndrome, (2) a totally flat response to TRH is rare, and (3) TSH suppression and lower than normal serum thyroid hormone levels are reversible after treatment. Since factors like severe systemic disease, diabetes mellitus and goitre also affect TSH secretion, they tend to obscure the statistically significant correlations between cortisol excess and TSH secretion.

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Section: Discussionmentioning

confidence: 51%

Tsh Secretion In Cushing's Syndrome: Relation To Glucocorticoid Excess, Diabetes, Goitre, And The ‘Sick Euthyroid Syndrome’

Benker¹,

Raida²,

Olbricht³

et al. 1990

Clinical Endocrinology

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“…Insulin also modulates thyroid hormone activity in some aspects (47,48). Interestingly, it was reported that TSH response to TRH injection failed in Type II diabetes patients (49). It seems likely that insulin and THs share the functions for some aspect of glucose metabolism, and they can regulate each other's expression.…”

Section: Discussionmentioning

confidence: 99%

Insulin Represses Transcription of the Thyroid Stimulating Hormone β-Subunit Gene through Increased Recruitment of Nuclear Factor I

Kim

Park

Song

et al. 2010

Journal of Biological Chemistry

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Although the regulation of thyroid stimulating hormone ␤-subunit gene (TSH␤) has been intensively studied, the functions of transcription factors involved are not fully understood. The authors found that the ؊615/؊516 promoter region of the TSH␤ interacts specifically with nuclear proteins derived from pituitary tissue or from cultured thyrotroph cells. The actual binding site at the nucleotide level, as revealed by DNase I protection assay, includes the consensus sequence for nuclear factor I (NFI). RT-PCR analysis indicated that NFI-B expression is restricted to thyrotroph cells in the anterior pituitary. EMSA and ChIP analysis showed that NFI-B binds most efficiently to the ؊588/؊560 region of TSH␤ promoter. The forced expressions of NFI-B markedly reduced TSH␤ promoter activity and its mRNA expression. Furthermore, it was also shown that the ؊588/؊560 region is involved in the insulin-mediated repression of the TSH␤. It was of particular interest to observe that NFI-B was recruited to the ؊588/؊560 region of the TSH␤ promoter in an insulin-dependent manner. Taken together, this study provides new insights of the delicate regulations of energy metabolism and hormonal homeostasis.

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“…The TRH test would be an option to detect intermediate defects. In fact, in patients with diabetes type 2 without pituitary disease and normal basal levels of TSH and free T4 and T3, this test detected impaired TSH secretion in approximately 38% of patients, considered as subclinical hypopituitarism [13].…”

Section: Subclinical Thyroid-stimulating Hormonedeficiencymentioning

confidence: 99%

“…There are studies that evaluated some isolated subclinical deficiencies. Subclinical thyroid-stimulating hormone (TSH) deficiency was reported in 20.3% of patients who were previously irradiated because of head and neck tumors [12] and in 38% of patients with type 2 diabetes [13], using the thyrotropic releasing hormone (TRH) test for diagnosis.…”

Section: Epidemiology Of Subclinical Hypopituitarismmentioning

confidence: 99%

An Update on Subclinical Hypopituitarism

Andújar-Plata¹,

Fern²,

ez-Rodriguez³

et al. 2016

J Steroids Horm Sci

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Subclinical deficiency of pituitary hormones represents an intermediate situation among normal pituitary secretion and overt hypopituitarism. Clinical hypopituitarism is associated with impaired morbidity and mortality, but there are not many studies on these topics in the subclinical setting. Moreover, clinical manifestations and diagnosis criteria are not well defined, so this entity is probably an underdiagnosed disorder. Long-term controlled studies are needed to establish a correct definition of subclinical hypopituitarism and to know its clinical implications, optimal methods of diagnosis, and indications for substitutive treatment. This review will focus on the evidence related to epidemiology, clinical manifestations, diagnosis, and treatment of subclinical hypopituitarism.

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Impaired thyrotrophin secretion following the administration of thyrotrophin-releasing hormone in type II diabetes mellitus

Abstract: Summary:Serum thyrotrophin has been measured before and after the intravenous administration of

Cited by 7 publications

References 14 publications

Tsh Secretion In Cushing's Syndrome: Relation To Glucocorticoid Excess, Diabetes, Goitre, And The ‘Sick Euthyroid Syndrome’

Tsh Secretion In Cushing's Syndrome: Relation To Glucocorticoid Excess, Diabetes, Goitre, And The ‘Sick Euthyroid Syndrome’

Insulin Represses Transcription of the Thyroid Stimulating Hormone β-Subunit Gene through Increased Recruitment of Nuclear Factor I

An Update on Subclinical Hypopituitarism

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