Previous studies demonstrated decreases in serum 25-hydroxyvitamin D in obese subjects. Studies were carried out to determine whiter serum vitamin D is low in obesity. The results indicate that serum vitamin D is significantly lower in obese than in nonobese individuals and may contribute to lower serum 25-hydroxyvitamin D in obesity.

The incidence of osteoporosis and fractures of the hip are diminished in blacks and in obese subjects. To determine whether bone mass is increased in them, bone mineral density (BMD) of the lumbar spine, trochanter, and femoral neck was measured by dual photon absorptiometry in 89 nonobese white and 51 nonobese black women, all of whom were within 30% of their ideal body weight and between the ages of 20 and 50 yr, and in 21 obese white women and 21 obese black women, all of whom weighed 30% on more than their ideal body weight and were in the same age range. The BMD of the mid radius was also measured by single photon absorptiometry. The mean BMD of the mid radius was higher in black than in white nonobese women [0.73 +/- 0.01 (+/- SE) vs. 0.70 +/- 0.01 g/cm2; P less than 0.01] and was not altered by obesity in either group. The mean BMD was higher in the black than in the white nonobese women at the lumbar spine (1.23 +/- 0.02 vs. 1.16 +/- 0.01 g/cm2; P less than 0.01), trochanter (0.78 +/- 0.02 vs. 0.72 +/- 0.01 g/cm2; P less than 0.01) and femoral neck (0.96 +/- 0.02 vs 0.90 +/- 0.02 g/cm2; P less than 0.02). The mean body weight was higher in the obese than in the nonobese white women (92 +/- 2 vs. 61 +/- 1 kg; P less than 0.001) and black women (94 +/- 3 vs. 63 +/- 1 kg; P less than 0.001). The mean BMD was higher in the obese than in the nonobese white women at the lumbar spine (1.24 +/- 0.03 g/cm2; P less than 0.05), trochanter (0.89 +/- 0.04; P less than 0.001), and femoral neck (0.99 +/- 0.03; P less than 0.01) and was higher in the obese than in the nonobese black women at the lumbar spine (1.33 +/- 0.03 g/cm2; P less tham 0.01), trochanter (0.88 +/- 0.04 g/cm2; P less than 0.05), and femoral neck (1.04 +/- 0.03 g/cm2; P less than 0.05). Multivariate regression analysis revealed positive correlations between body weight and BMD at each of the 3 weight-bearing sites, but not at the mid radius, in both the black women and white women.(ABSTRACT TRUNCATED AT 400 WORDS)

Menopause and estrogen deficiency are associated with apparent intestinal resistance to vitamin D, which can be reversed by estrogen replacement. The in vivo influence of estrogens on duodenal vitamin D receptor (VDR) was studied in three groups of rats: ovariectomized (OVX), sham-operated, and ovariectomized rats treated daily with estrogen (40 g/kg BW) for 2 weeks (OVX ϩ E). Estrogen administration to OVX rats resulted in a 2-fold increase in VDR messenger RNA transcripts. 1,25(OH) 2 D 3 was shown to bind specifically to one class of receptors in duodenal mucosal extracts, with a dissociation constant of 0.03 nM. Binding was significantly increased in duodenal extracts from OVX ϩ E rats, compared with OVX rats (735 Ϯ 81 vs. 295 Ϯ 26 fmol/mg protein; P Ͻ 0.001); a comparable, 1.5-to 2-fold increase in VDR protein expression was observed in Western blot analyzes of the duodenal mucosa. Markers of VDR activity were increased in estrogen-exposed rats: calbindin-9k messenger RNA transcript content was 1.4-to 1.6-fold higher, and alkaline phosphatase activity was 1.4-to 3-fold higher in sham-operated and OVX ϩ E, respectively, compared with OVX. 25(OH)D, 1,25(OH) 2 D, or PTH levels were not altered by estrogen treatment. Cumulatively, these findings suggest that estrogen up-regulates VDR expression in the duodenal mucosa and concurrently increases the responsiveness to endogenous 1,25(OH) 2 D. Modulation of intestinal VDR activity by estrogen, and subsequent influence on intestinal calcium absorption, could be one of the major protective mechanisms of estrogen against osteoporosis. (Endocrinology 140: 280 -285, 1999) I NTESTINAL calcium absorption takes place via two main mechanisms: passive diffusion, which occurs when luminal calcium is high; and active absorption, a complex and not fully understood process mediated by 1,25(OH) 2 D 3 , which predominates when luminal calcium is low (1). Under physiological circumstances, 1,25(OH) 2 D 3 is primarily produced in the kidneys under the influence of PTH stimulation. PTH secretion, in turn, is dependent on extracellular free calcium concentration, as sensed by calcium-sensing-receptors located in parathyroid cells' membranes (2). Overall, the rate of active intestinal calcium absorption is determined by physiologic interactions between various components of the PTH-vitamin D-endocrine system organized in a multilevel negative feed-back loop structure.Intestinal calcium absorption declines with age, both in humans (3, 4) and in rats (5). A widely held hypothesis suggests that the decrease in intestinal calcium absorption results from a sequence of events initiated by low estrogen levels, causing increased bone resorption; released calcium increases extracellular space calcium concentration, which suppresses PTH secretion, followed by a subsequent decrease in 1,25(OH) 2 D 3 production and in 1,25(OH) 2 D 3 plasma concentration, and finally results in decreased intestinal calcium absorption (6).Nevertheless, there is evidence that estrogen may be more directly i...

To evaluate the effect of dietary fiber supplements on levothyroxine (T4) bioavailability in hypothyroid patients, dietary fiber-containing supplementation was withheld from patients requiring disproportionately high doses of T4, in whom a dietary history revealed ingestion of a dietary fiber supplement. The dose of T4 was maintained at a constant level. Serum thyrotropin (TSH) was assessed before and after removal of the dietary fiber supplements. T4 requirements, reflected by either decreased serum TSH or by decreased T4 dose, was observed in conjunction with decreased dietary fiber intake compared with T4 requirement during increased dietary fiber intake. In vitro experiments carried out to determine the mechanism of interaction between dietary fiber and T4 revealed dose dependent, nonspecific adsorption of levothyroxine by wheat bran. These results indicate a decrease in T4 bioavailability by dietary fiber through a mechanism involving nonspecific adsorption of T4 to dietary fibers. Increased intake of dietary fiber may account for the need for larger than expected doses of T4 in some hypothyroid patients.