Orchiectomy and response to testosterone in the development of obesity in young Otsuka-Long-Evans-Tokushima Fatty (OLETF) rats

Shimizu, Hiroyuki; Ohtani, Ken-Ichi; Uehara, Yutaka; Abe, Yoshinao; Takahashi, Hiroki; Tsuchiya, Takafumi; Sato, Noriyuki; Ibuki, Yoshito; Mori, Masataka

doi:10.1038/sj.ijo.0800586

Cited by 19 publications

(10 citation statements)

References 25 publications

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“…Castration reduces and T stimulates body weight gain, nitrogen retention, and/or food intake in a number of species [73, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84]. As mentioned previously, intact male sheep exhibit increased numbers of cells expressing NPY and increased NPY mRNA during long days that are associated with increased voluntary food intake [23].…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y Gene Expression in Male Sheep: Influence of Photoperiod and Testosterone

Dobbins

Lubbers²,

Jackson³

et al. 2004

Neuroendocrinology

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The frequency of pulsatile release of gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) is high in the breeding season and low in the nonbreeding season. These alterations in the patterns of GnRH and LH release are due to an interaction of daylength and gonadal steroid negative feedback. A vast amount of data indicates that steroid-responsive neural systems may play a role in regulating seasonal changes in GnRH release. One candidate system is neuropeptide Y (NPY). To determine the independent and interactive influences of photoperiod and steroid exposure on NPY mRNA levels, we used hypothalamic tissue from four groups (n = 4 per group) of castrated male sheep that were simultaneously housed in photochambers and exposed to: (1) a 16L:8D photoperiod (LD); (2) LD and implanted with testosterone (LD + T); (3) a 10L:14D photoperiod (SD), and (4) SD + T. Circulating levels of T averaged 2.8 ± 0.2 ng/ml in implanted animals, but were undetectable in nonimplanted males. Mean LH levels were significantly reduced (p < 0.01) in the LD + T group as compared with the other groups which did not differ from each other. The silver grain area per NPY neuron in the arcuate nucleus, as assessed by in situ hybridization, was inversely related to mean LH values, with the grain area per cell being significantly greater (p < 0.05) for LD + T males than for all other groups which did not differ from each other. NPY cell numbers were not significantly different (p > 0.10) among the treatment groups. These results show that NPY mRNA expression is increased in male sheep during a LD photoperiod in a T-dependent manner. Our data are consistent with the idea that NPY is involved in the seasonal regulation of GnRH and LH release in the male sheep.

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Section: Discussionmentioning

confidence: 99%

Neuropeptide Y Gene Expression in Male Sheep: Influence of Photoperiod and Testosterone

Dobbins

Lubbers²,

Jackson³

et al. 2004

Neuroendocrinology

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“…In contrast, Shimizu et al. (124) showed that serum leptin levels were decreased by orchiectomy in fatty rats, and testosterone supplement reversed this decrease. Nazian (125) showed that serum leptin rises in male rats from immaturity to young adults as the serum testosterone also rises.…”

Section: Transcriptional Regulation Of Proteins In Adipose Tissues Bymentioning

confidence: 92%

Direct effects of sex steroid hormones on adipose tissues and obesity

2004

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Sex steroid hormones are involved in the metabolism, accumulation and distribution of adipose tissues. It is now known that oestrogen receptor, progesterone receptor and androgen receptor exist in adipose tissues, so their actions could be direct. Sex steroid hormones carry out their function in adipose tissues by both genomic and nongenomic mechanisms. In the genomic mechanism, the sex steroid hormone binds to its receptor and the steroid-receptor complex regulates the transcription of given genes. Leptin and lipoprotein lipase are two key proteins in adipose tissues that are regulated by transcriptional control with sex steroid hormones. In the nongenomic mechanism, the sex steroid hormone binds to its receptor in the plasma membrane, and second messengers are formed. This involves both the cAMP cascade and the phosphoinositide cascade. Activation of the cAMP cascade by sex steroid hormones would activate hormone-sensitive lipase leading to lipolysis in adipose tissues. In the phosphoinositide cascade, diacylglycerol and inositol 1,4,5-trisphosphate are formed as second messengers ultimately causing the activation of protein kinase C. Their activation appears to be involved in the control of preadipocyte proliferation and differentiation. In the presence of sex steroid hormones, a normal distribution of body fat exists, but with a decrease in sex steroid hormones, as occurs with ageing or gonadectomy, there is a tendency to increase central obesity, a major risk for cardiovascular disease, type 2 diabetes and certain cancers. Because sex steroid hormones regulate the amount and distribution of adipose tissues, they or adipose tissue-specific selective receptor modulators might be used to ameliorate obesity. In fact, hormone replacement therapy in postmenopausal women and testosterone replacement therapy in older men appear to reduce the degree of central obesity. However, these therapies have numerous side effects limiting their use, and selective receptor modulators of sex steroid hormones are needed that are more specific for adipose tissues with fewer side effects.

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“…Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats exhibit either reduced (94) or no changes (53) in testosterone or estradiol levels. It is highly likely that changes in sex hormone levels are species and strain-specific, which may be one of the reasons for the somewhat conflicting data in rodents.…”

Section: Sex Hormones and Type II Diabetesmentioning

confidence: 99%

Sex, diabetes and the kidney

Maric¹

2009

American Journal of Physiology-Renal Physiology

116

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The incidence and the rate of progression of nondiabetic renal disease is generally greater in men compared with age-matched women, suggesting that the female sex is protective and/or that the male sex is a risk factor for the development and progression of nondiabetic renal disease. In diabetes, even though the male sex still appears to be a risk factor, this relationship is not as strong as it is in nondiabetic renal disease. Experimental evidence suggests that both estrogens and androgens play an important role in the pathophysiology of renal disease. Thus one of the potential mechanisms for the absence of a clear sex difference in the setting of diabetes may be alterations in sex hormone levels. Indeed, studies suggest that diabetes is a state of an imbalance in sex hormone levels; however, whether these changes correlate with the decline in renal function associated with diabetes is unclear. Furthermore, diabetic renal disease rarely develops before puberty, and the onset of puberty accelerates microalbuminuria, supporting the idea of the involvement of sex hormones in the development and progression of the disease. However, other than a handful of experimental studies indicating that treatment with or removal of sex hormones alters the course of diabetic renal disease, very few studies have actually directly examined the correlation between sex hormones and the disease development and progression. Further studies are necessary to determine the precise contribution of sex hormones in the pathophysiology of diabetic renal disease to develop novel and potentially sex-specific therapeutic treatments.

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Orchiectomy and response to testosterone in the development of obesity in young Otsuka-Long-Evans-Tokushima Fatty (OLETF) rats

Cited by 19 publications

References 25 publications

Neuropeptide Y Gene Expression in Male Sheep: Influence of Photoperiod and Testosterone

Neuropeptide Y Gene Expression in Male Sheep: Influence of Photoperiod and Testosterone

Direct effects of sex steroid hormones on adipose tissues and obesity

Sex, diabetes and the kidney

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