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.

SUMMARY: In males, visceral obesity and androgen deficiency often present together and result in harmful effects on bone. Our findings show that both factors are independently associated with adverse effects on femoral bone structure and strength, and trenbolone protects rats from diet-induced visceral obesity and consequently normalises femoral bone structural strength. INTRODUCTION: In light of the rapidly increasing incidence of obesity and osteoporosis globally, and recent conjecture regarding the effects of visceral adiposity and testosterone deficiency on bone health, we investigated the effects of increased visceral adipose tissue (VAT) mass on femoral bone mineral density (BMD), structure and strength in normal weight rats with testosterone deficiency. METHODS: Male Wistar rats (n = 50) were fed either standard rat chow (CTRL, n = 10) or a high-fat/high-sugar diet (HF/HS, n = 40). Following 8 weeks of feeding, rats underwent sham surgery (CTRL, n = 10; HF/HS, n = 10) or orchiectomy (HF/HS + ORX, n = 30). Following a 4-week recovery period, mini-osmotic pumps containing either vehicle (CTRL, n = 10; HF/HS, n = 10; HF/HS + ORX, n = 10), 2.0 mg kg day(-1), testosterone (HF/HS + ORX + TEST, n = 10) or 2.0 mg kg day(-1) trenbolone (HF/HS + ORX + TREN, n = 10) were implanted for 8 weeks of treatment. Dual-energy X-ray absorptiometry and three-point bending tests were used to assess bone mass, structure and strength of femora. RESULTS: Diet-induced visceral obesity resulted in decreased bone mineral area (BMA) and content (BMC) and impaired femoral stiffness and strength. Orchiectomy further impaired BMA, BMC and BMD and reduced energy to failure in viscerally obese animals. Both TEST and TREN treatment restored BMA, BMC, BMD and energy to failure. Only TREN reduced visceral adiposity and improved femoral stiffness and strength. CONCLUSIONS: Findings support a role for both visceral adiposity and testosterone deficiency as independent risk factors for femoral osteoporosis, adverse bone geometry and impaired bone strength in male rats. Trenbolone may be a more effective candidate for androgen replacement therapy than testosterone in viscerally obese testosterone-deficient males.

Medical treatment of cholangiohepatitis and cholelithiasis in mature horses: 9 cases (1991-1998).

The medical approach to treatment of cholangiohepatitis and cholelithiasis in 9 horses is described. Seven horses were treated successfully and returned to normal use, with a minimum follow-up period of 12 months. Long-term antimicrobial therapy was believed to be critical in those cases that survived, with a median treatment duration of 51 days (range 17-124 days). Treatment failure was associated with severe periportal and bridging hepatic fibrosis from biopsy material obtained at admission in 2 horses, one of whom also presented with hyperammonaemic hepatic encephalopathy. Transabdominal ultrasound was used diagnostically in each case to obtain hepatic biopsy material for histopathology and bacterial culture, to evaluate hepatic size and echogenicity and to identify and monitor the dissolution of hepatoliths. Histologically, all horses had evidence of suppurative cholangiohepatitis with varying degrees of periportal and bridging fibrosis. Discrete hyperechoic calculi were identified in 4 cases, but all horses had ultrasonographic evidence of biliary obstruction with numerous dilated bile ducts. Aerobic and anaerobic cultures of liver biopsy material were negative from 7 horses, but 2 different species of Escherichia coli were obtained from one horse, and Bacteroides vulgatus and Escherichia coli were isolated from another. In all 7 horses that survived, clinical recovery was seen before normalisation of biochemical indices of hepatobiliary function including gammaglutamyl transaminopeptidase (GGT), alkaline phosphatase (AP), bile acids and serum bilirubin. Serum GGT levels were monitored extensively as a marker of hepatobiliary disease and actually increased during the initial period of clinical improvement in horses that recovered. Supportive medical therapy with i.v. fluids was also a critical part of the therapy of several cases in this report, both acutely and in the management of chronic cases that deteriorated clinically during treatment. Previous therapeutic failures may well be related to treatment periods of inadequate duration, and the authors recommend that antimicrobial therapy should be continued until GGT values are normal.