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

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

doi:10.1385/endo:27:3:301

Cited by 13 publications

(11 citation statements)

References 25 publications

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“…Experimental and clinical studies showed that this imbalance in sex hormone levels in men with type 1 diabetes (18,35) and male streptozotocin (STZ)-induced diabetic rats (18,35) is associated with the progression of diabetic renal disease. Similar to males, diabetic females also exhibit an imbalance in sex hormone levels, albeit in the opposite direction: decreased estradiol and increased testosterone levels (19,27). The changes in the balance in sex hormone levels in both males and females support that concept that sex hormones may play a role in the pathogenesis of diabetic renal disease.…”

mentioning

confidence: 54%

Inhibition of estradiol synthesis attenuates renal injury in male streptozotocin-induced diabetic rats

Manigrasso

Sawyer

Marbury

et al. 2011

American Journal of Physiology-Renal Physiology

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We previously showed that the male streptozotocin (STZ)-induced diabetic rat exhibits decreased circulating testosterone and increased estradiol levels. While supplementation with dihydrotestosterone is partially renoprotective, the aim of the present study was to examine whether inhibition of estradiol synthesis, by blocking the aromatization of testosterone to estradiol using an aromatase inhibitor, can also prevent diabetes-associated renal injury. The study was performed on male Sprague-Dawley nondiabetic, STZ-induced diabetic, and STZ-induced diabetic rats treated with 0.15 mg/kg of anastrozole, an aromatase inhibitor (Da) for 12 wk. Treatment with anastrozole reduced diabetes-associated increases in plasma estradiol by 39% and increased plasma testosterone levels by 187%. Anastrozole treatment also attenuated urine albumin excretion by 42%, glomerulosclerosis by 30%, tubulointerstitial fibrosis by 32%, along with a decrease in the density of renal cortical CD68-positive cells by 50%, and protein expression of transforming growth factor-β by 20%, collagen type IV by 29%, tumor necrosis factor-α by 28%, and interleukin-6 by 25%. Anastrozole also increased podocin protein expression by 18%. We conclude that blocking estradiol synthesis in male STZ-induced diabetic rats is renoprotective.

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mentioning

confidence: 54%

Inhibition of estradiol synthesis attenuates renal injury in male streptozotocin-induced diabetic rats

Manigrasso

Sawyer

Marbury

et al. 2011

American Journal of Physiology-Renal Physiology

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“…Specifically, men have low testosterone and high estradiol levels [74][75][76] in contrast to women who exhibit low estradiol and higher testosterone levels. 77,78 An imbalance in sex hormone levels as well as differential expression of renal estrogen and androgen receptors by sex has been reported in experimental models of DKD. [79][80][81] Several studies have also suggested that restoring the sex hormone imbalance may be an effective treatment for DKD.…”

Section: Contribution Of Sex Hormones To Dkdmentioning

confidence: 99%

Sex Differences in Diabetic Kidney Disease

Maric‐Bilkan

2020

Mayo Clinic Proceedings

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While the global prevalence of both type 1 and type 2 diabetes mellitus is similar in men and women, the consequences of diabetes on associated end-organ complications, including diabetic kidney disease appear to be more sex-specific. Particularly, women with diabetes have higher mortality rates for diabetes-related deaths, and higher prevalence of diabetic kidney disease risk factors such as hypertension, hyperglycemia, obesity, and dyslipidemia. However, the evidence for the impact of sex on diabetic kidney disease prevalence and disease progression is limited and inconsistent. Although most studies agree that the protective effect of the female sex against the development of kidney disease is diminished in the setting of diabetes, the reasons for this observation are unclear. Whether or not sex differences exist in the risk of diabetic kidney disease is also unclear, with studies reporting either higher risk in men, women, or no sex differences. Despite the remaining controversies, some of the factors that associate with sex differences in the risk of diabetic kidney disease are age at onset, and type and duration of diabetes. There is growing appreciation of the importance of sex hormones in the regulation of renal function, with estrogens generally considered to be renoprotective. Although some progress has been made towards better understanding of the mechanisms by which sex hormones play a role in the pathophysiology of diabetic kidney disease, the translational potential

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

Cited by 13 publications

References 25 publications

Inhibition of estradiol synthesis attenuates renal injury in male streptozotocin-induced diabetic rats

Inhibition of estradiol synthesis attenuates renal injury in male streptozotocin-induced diabetic rats

Sex Differences in Diabetic Kidney Disease

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

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