Changes in ovarian steroidogenesis in insulin-resistant, type 2 diabetic Goto–Kakizaki rats after thyroidectomy and gonadotropin treatment

Tamura, Kazuhiro; Osada, Shingo; Matsushita, Mayumi; Abe, Keiko; Kuroda, Hiroshi

doi:10.1016/j.ejphar.2005.02.048

Cited by 3 publications

(1 citation statement)

References 36 publications

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“…Although there are reports about the effects of hypothyroidism in the type 1 (Hibbe et al, 1991) and type 2 diabetic models (Matsushita et al, 2005; Tamura et al, 2005; Hwang et al, 2009), no studies have been reported about the effects of hypothyroidism in type 2 diabetic model on cell proliferation and neuroblast differentiation. In the present study, we investigated the consequences of adult-onset hypothyroidism in diabetic rats using methimazole, an anti-thyroid drug, which has been used in the management of hyperthyroid patients (Cooper 2005).…”

Section: Introductionmentioning

confidence: 99%

Effects of hypothyroidism on cell proliferation and neuroblasts in the hippocampal dentate gyrus in a rat model of type 2 diabetes

Hwang

Choi

et al. 2010

Anat Cell Biol

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We observed how the hypothyroid state affects diabetic states and modifies cell proliferation and neuroblast differentiation in the hippocampal dentate gyrus (DG). For this, 0.03% methimazole, an anti-thyroid drug, was administered to 7-week-old, pre-diabetic Zucker diabetic fatty (ZDF) rats by drinking water for 5 weeks, and the animals were sacrificed at 12 weeks of age. At this age, corticosterone levels were significantly increased in the ZDF rats compared to those in the control (Zucker lean control, ZLC) rats. Methimazole (methi) treatment in the ZDF rats (ZDF-methi rats) significantly decreased corticosterone levels and diabetes-induced hypertrophy of adrenal glands. In the DG, Ki67 (a marker for cell proliferation)- and doublecortin (DCX, a marker for neuronal progenitors)-immunoreactive cells were much lower in the ZDF rats than those in the ZLC rats. However, in ZDF-methi rats, numbers of Ki67- and DCX-immunoreactive cells were similar to those in the ZLC rats. These suggest that methi significantly reduces diabetes-induced hypertrophy of the adrenal gland and alleviates the diabetes-induced reduction of cell proliferation and neuronal progenitors in the DG.

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Section: Introductionmentioning

confidence: 99%

Effects of hypothyroidism on cell proliferation and neuroblasts in the hippocampal dentate gyrus in a rat model of type 2 diabetes

Hwang

Choi

et al. 2010

Anat Cell Biol

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Effect of Troglitazone on the Excess Testosterone and LH Secretion in Thyroidectomized, Insulin-Resistant, Type 2 Diabetic Goto–Kakizaki Rats

Matsushita

Tamura

Osada

et al. 2005

ENDO

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Our previous study suggested that hypothyroidism in Goto-Kakizaki (GK) rats with insulin resistance and type 2 diabetes elevates their serum testosterone and luteinizing hormone (LH) levels and ovarian LH receptor messenger RNA (mRNA) expression. The present study assessed the effects of troglitazone (Tro), an insulin-sensitizing agent, on these hypothyroidism-induced hormonal changes in GK rats. GK and normal (Wistar strain) female rats were thyroidectomized (Tx) and then injected with 5 IU of equine chorionic gonadotropin (eCG) for 5 d starting 1 wk after thyroidectomy (the control groups). In the test groups, Tx GK and Wistar rats were injected with both eCG and Tro (100 mg kg-1) po for 5 d. Tro treatment had no effect on the elevated LH serum levels in eCG-treated Tx GK rats but suppressed their enhanced serum testosterone levels as well as significantly decreasing their LH receptor mRNA expression. Tro lowered testosterone and LH receptor mRNA levels in cultured theca cells. These results indicate that Tro lowers the elevated testosterone secretion and ovarian LH receptor mRNA expression that is induced in GK rats by Tx and gonadotropin treatment, which suggests that insulin resistance may be involved in enhancing testosterone production and LH receptor expression in the ovary.

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Sex-Related Aspects in Diabetic Kidney Disease—An Update

Löffler

Ziller

2023

JCM

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Differences between the sexes exist in many diseases, and in most cases, being a specific sex is considered a risk factor in the development and/or progression. This is not quite so clear in diabetic kidney disease (DKD), the development and severity of which depends on many general factors, such as the duration of diabetes mellitus, glycemic control, and biological risk factors. Similarly, sex-specific factors, such as puberty or andro-/menopause, also determine the microvascular complications in both the male and female sex. In particular, the fact that diabetes mellitus itself influences sex hormone levels, which in turn seem to be involved in renal pathophysiology, highlights the complexity of the question of sex differences in DKD. The major objective of this review is to summarize and simplify the current knowledge on biological sex-related aspects in the development/progression but also treatment strategies of human DKD. It also highlights findings from basic preclinical research that may provide explanations for these differences.

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Changes in ovarian steroidogenesis in insulin-resistant, type 2 diabetic Goto–Kakizaki rats after thyroidectomy and gonadotropin treatment

Cited by 3 publications

References 36 publications

Effects of hypothyroidism on cell proliferation and neuroblasts in the hippocampal dentate gyrus in a rat model of type 2 diabetes

Effects of hypothyroidism on cell proliferation and neuroblasts in the hippocampal dentate gyrus in a rat model of type 2 diabetes

Effect of Troglitazone on the Excess Testosterone and LH Secretion in Thyroidectomized, Insulin-Resistant, Type 2 Diabetic Goto–Kakizaki Rats

Sex-Related Aspects in Diabetic Kidney Disease—An Update

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