Chronic Alcohol Treatment Results in Disturbed Vitamin D Metabolism and Skeletal Abnormalities in Rats

Abstract

The effect of chronic alcohol consumption on the skeleton was investigated in rats. The treated group received ethanol administered as 38% of caloric intake in a liquid diet (Sustacal) for 10 months. The control rats were pair weighted to the ethanol-treated animals throughout the study; the growth curves of the two groups were the same. The controls were given the same liquid diet except that dextrin:maltose (3:1) was substituted isocalorically for ethanol. Ethanol-treated rats did not differ from the pair-weighted controls in mean serum calcium, phosphorous, or creatinine. In contrast, serum magnesium was reduced (p less than 0.02) in alcohol-treated rats. Ethanol treatment also resulted in changes in the serum concentrations of vitamin D metabolites; serum 25-hydroxyvitamin D3 was increased (p less than 0.001), while serum 1,25-dihydroxyvitamin D3 was decreased (p less than 0.01). Tibial length was reduced in ethanol-treated rats (p less than 0.05) but there was no change in femoral length. Medullary area was increased in tibial diaphyses from alcohol-treated rats compared to weight matched control animals (p less than 0.01), indicating a net increase in resorption. The cross-sectional area of the tibial diaphysis of ethanol-treated rats was the same as the matched controls. Trabecular bone was decreased in the tibial metaphysis of ethanol-treated rats compared to the matched controls (p less than 0.05) indicating a net loss of trabecular bone. Ethanol treatment did not have an effect on the organic weight of the femur but the ash weight was reduced (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Vitamin D Supplementation Protects against Bone Loss Associated with Chronic Alcohol Administration in Female Mice

“…A recent comprehensive study in alcoholic patients reported that nutritional status and low 1,25(OH) 2 D 3 plasma concentrations are independently related to increased prevalence of rib and vertebral fractures (Gonzá lez-Reimers et al, 2011). In rodent models, we and others have reported similar decreases in circulating 1,25(OH) 2 D 3 after chronic EtOH exposure (Turner et al, 1988;Keiver et al, 1996;Shankar et al, 2006). In addition, we have reported that this decrease in serum 1,25(OH) 2 D 3 is associated with a significant increase in renal CYP24A1, the enzyme responsible for the conversion of 1,25(OH) 2 D 3 to inactive 1,24,25-hydroxyvitamin D 3 metabolite (Shankar et al, 2008b).…”

“…In addition, we have reported that this decrease in serum 1,25(OH) 2 D 3 is associated with a significant increase in renal CYP24A1, the enzyme responsible for the conversion of 1,25(OH) 2 D 3 to inactive 1,24,25-hydroxyvitamin D 3 metabolite (Shankar et al, 2008b). It is noteworthy that we and others have also reported increases, decreases, or no change in serum concentrations of 25OHD 3 after EtOH consumption in rodents (Turner et al, 1988;Wezeman et al, 2007;Shankar et al, 2008b).…”

Effects of low-dose parathyroid hormone on bone mass, turnover, and ectopic osteoinduction in a rat model for chronic alcohol abuse

“…The detrimental effects on bone metabolism that we observed are consistent with earlier studies [39][40][41][42]. Alcohol is a potent inhibitor of bone growth in rats and decreases peak bone mass [39][40][41][42].…”

Alcohol Drinking Patterns and Nutrition in Alcoholic Liver Disease

“…Similar reduction of plasma 1,25 dihydroxyvitamin D3 levels were also found in animal studies after chronic ethanol exposure (Turner et al 1988). Reduction of circulating vitamin D levels in alcohol abusers may lead to reduced bone mass and lower calcium levels (Sampson, 1997;Keiver and Weinberg, 2003).…”