The effects of visceral obesity and androgens on bone: trenbolone protects against loss of femoral bone mineral density and structural strength in viscerally obese and testosterone-deficient male rats

Donner, D.; Elliott, Grace E.; Beck, Belinda R.; Forwood, Mark R.; Toit, Eugene F. Du

doi:10.1007/s00198-015-3345-1

Cited by 8 publications

(8 citation statements)

References 47 publications

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“…Consistent with these findings in humans, HFD-induced obesity lowers bone quality measures in rodents, but in animal studies, HFD is often associated with lowered BMD and BMC at various sites including total body, tibia, femur and spine in the majority of rodent studies [106–118] (Supplemental Table S1). Although several studies actually show a greater BMD attributed to high fat feeding [119–124] (Supplemental Table S1).…”

Section: Dietary Energy and Fat On Bone In Preclinical Studiesmentioning

confidence: 54%

Obesity is a concern for bone health with aging

2017

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Accumulating evidence supports a complex relationship between adiposity and osteoporosis in overweight/obese individuals, with local interactions and endocrine regulation by adipose tissue on bone metabolism and fracture risk in elderly populations. This review was conducted to summarize existing evidence to test the hypothesis that obesity is a risk factor for bone health in aging individuals. Mechanisms by which obesity adversely affects bone health are believed to be multiple, such as an alteration of bone-regulating hormones, inflammation, oxidative stress, the endocannabinoid system, that affect bone cell metabolism are discussed. In addition, evidence on the effect of fat mass and distribution on bone mass and quality is reviewed together with findings relating energy and fat intake with bone health. In summary, studies indicate that the positive effects of body weight on bone mineral density cannot counteract the detrimental effects of obesity on bone quality. However, the exact mechanism underlying bone deterioration in the obese is not clear yet and further research is required to elucidate the effect of adipose depots on bone and fracture risk in the obese population.

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Section: Dietary Energy and Fat On Bone In Preclinical Studiesmentioning

confidence: 54%

Obesity is a concern for bone health with aging

2017

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“…However, it has been shown previously that testosterone deprivation alone could cause osteoporosis (Tuck & Francis 2009). Moreover, the recent study by Donner et al (2015) demonstrated that dietinduced visceral obesity resulted in decreased bone mineral area and content and impaired femoral stiffness and strength without changes in testosterone levels. All of these findings indicated that either obesity or testosterone deprivation could lead to osteoporosis.…”

Section: Discussionmentioning

confidence: 99%

Obesity does not aggravate osteoporosis or osteoblastic insulin resistance in orchiectomized rats

Potikanond¹,

Rattanachote²,

Pintana³

et al. 2016

Journal of Endocrinology

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The present study aimed to test the hypothesis that testosterone deprivation impairs osteoblastic insulin signaling, decreases osteoblast survival, reduces bone density, and that obesity aggravates those deleterious effects in testosterone-deprived rats. Twenty four male Wistar rats underwent either a bilateral orchiectomy (O, nZ12) or a sham operation (S, nZ12). Then the rats in each group were further divided into two subgroups fed with either a normal diet (ND) or a high-fat diet (HF) for 12 weeks. At the end of the protocol, blood samples were collected to determine metabolic parameters and osteocalcin ratios. The tibiae were collected to determine bone mass using microcomputed tomography and for osteoblast isolation. The results showed that rats fed with HF (sham-operated HF-fed rats (HFS) and ORX HF-fed rats (HFO)) developed peripheral insulin resistance and had decreased trabecular bone density. In ND-fed rats, only the ORX ND-fed rats (NDO) group had decreased trabecular bone density. In addition, osteoblastic insulin resistance, as indicated by a decrease in tyrosine phosphorylation of the insulin receptor and Akt, were observed in all groups except the sham-operated ND-fed rats (NDS) rats. Those groups, again with the exception of the NDS rats, also had decreased osteoblastic survival. No differences in the levels of osteoblastic insulin resistance and osteoblastic survival were found among the NDO, HFS, and HFO groups. These findings suggest that either testosterone deprivation or obesity alone can impair osteoblastic insulin signaling and decrease osteoblastic survival leading to the development of osteoporosis. However, obesity does not aggravate those deleterious effects in the bone of testosterone-deprived rats.

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“…As we have demonstrated previously with similar models (35,46), we propose that the HF/HSϩORX model used in the present study is an appropriate representation of males with TEST-deficient MetS.…”

Section: Characteristics Of the Test-deficient Mets Modelmentioning

confidence: 78%

“…Additionally, TREN causes a more potent reduction in retroperitoneal/visceral fat pad mass than TEST in hypogonadic male rats (34,35). More recently, we have shown that TREN improves multiple components of the MetS and improves myocardial tolerance to I-R in normogonadic rats (36).…”

mentioning

confidence: 94%

Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome

et al. 2016

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The increasing prevalence of obesity adds another dimension to the pathophysiology of testosterone (TEST) deficiency (TD) and potentially impairs the therapeutic efficacy of classical TEST replacement therapy. We investigated the therapeutic effects of selective androgen receptor modulation with trenbolone (TREN) in a model of TD with the metabolic syndrome (MetS). Male Wistar rats (n=50) were fed either a control standard rat chow (CTRL) or a high-fat/high-sucrose (HF/HS) diet. After 8 weeks of feeding, rats underwent sham surgery or an orchiectomy (ORX). Alzet miniosmotic pumps containing either vehicle, 2-mg/kg·d TEST or 2-mg/kg·d TREN were implanted in HF/HS+ORX rats. Body composition, fat distribution, lipid profile, and insulin sensitivity were assessed. Infarct size was quantified to assess myocardial damage after in vivo ischaemia reperfusion, before cardiac and prostate histology was performed. The HF/HS+ORX animals had increased sc and visceral adiposity; circulating triglycerides, cholesterol, and insulin; and myocardial damage, with low circulating TEST compared with CTRLs. Both TEST and TREN protected HF/HS+ORX animals against sc fat accumulation, hypercholesterolaemia, and myocardial damage. However, only TREN protected against visceral fat accumulation, hypertriglyceridaemia, and hyperinsulinaemia and reduced myocardial damage relative to CTRLs. TEST caused widespread cardiac fibrosis and prostate hyperplasia, which were less pronounced with TREN. We propose that TEST replacement therapy may have contraindications for males with TD and obesity-related MetS. TREN treatment may be more effective in restoring androgen status and reducing cardiovascular risk in males with TD and MetS.

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The effects of visceral obesity and androgens on bone: trenbolone protects against loss of femoral bone mineral density and structural strength in viscerally obese and testosterone-deficient male rats

Cited by 8 publications

References 47 publications

Obesity is a concern for bone health with aging

Obesity is a concern for bone health with aging

Obesity does not aggravate osteoporosis or osteoblastic insulin resistance in orchiectomized rats

Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome

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