Calcitropic Hormones and Metabolic Markers Differ in Young South Asian Indian Men and Caucasians (P04-119-19)

Objectives The incidence rate of metabolic syndrome is higher in South Asian Indians (SAI) and is generally accompanied by changes in calcitropic hormones. Typically, these findings are reported in middle age or older adults and data in a younger population is scarce. The purpose of the study was to analyze the differences in calcitropic hormones and metabolic markers in younger South Asian Indian and Caucasian men Methods Caucasian or South Asian Indian men between 21–41 years of age were recruited for this study. Anthropometric measurements such as weight (kg), height (cm) and waist circumference (cm) were obtained. An 8-hour fasting blood sample was collected for analysis of serum concentrations of 25 hydroxyvitamin D (25OHD), parathyroid hormone (PTH), C-reactive protein (CRP), osteocalcin (OC), high molecular weight (HMW) adiponectin, glycemic indices, and lipid profile. Independent sample t-tests were used to report the mean differences between groups. The significance level was set for P < 0.05. Results A total of 26 men (13 SAIs and 13 Caucasians) completed the study. The mean age for SAI men was 27.82 ± 5.64 y and 27.39 ± 5.29 y for Caucasian men. Body mass index (BMI) averaged at 25.93 ± 3.97 kg/m2 for SAIs and 26.44 ± 2.49 kg/m2 for Caucasians. Serum 25(OH)D concentrations were lower in the SAI men (21.58 ± 8.11 ng/mL) compared to Caucasian men (29.14 ± 7.17 ng/mL) (P = 0.019). Serum concentrations of PTH were higher (P = 0.007) in the SAI men (72.39 ± 24.32 pg/mL) compared to Caucasian Men (45.30 ± 21.95 pg/mL). Furthermore, HMW adiponectin was significantly lower (P = 0.008) in SAIs (2.00 ±1.29 mg/L) compared to Caucasians (3.95 ± 2.01 mg/L). Glycemic indices, inflammatory markers, serum osteocalcin, and lipid profiles were not different between groups. Conclusions These results show that differences in calcitropic hormones are observed in young South Asian Indian men compared to Caucasians although differences in metabolic parameters do not exist at this point. Changes in calcitropic hormones may provide early insight into the development of metabolic syndrome in this population. Intervention studies should address whether correction of vitamin D status will delay the development of metabolic syndrome in this population. Funding Sources CNHP Seed Funding.

Changes of macrominerals and calcitropic hormones in serum of periparturient dairy cows subject to subclinical hypocalcaemia

The aims of the study reported in the Research Communication were to evaluate changes of macrominerals and major calcitropic hormone concentrations in 51 healthy dairy cows over the peripartum period, and to compare those cows with 51 cows subject to subclinical hypocalcaemia (SCH) on calving day. The results showed that serum calcium (Ca) and potassium (K) concentrations were lowest in the healthy periparturient dairy cows at parturition, while sodium (Na) and parathyroid hormone (PTH) concentrations were highest. Serum magnesium (Mg), chloride (Cl) and phosphorus (P) concentrations were highest 1 wk prepartum, however, the concentration of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] was highest 1 wk postpartum. The dairy cows with subclinical hypocalcaemia (SCH) had significantly lower serum levels of Ca, K, Na, Mg, Cl, 1,25(OH)2D3 and glucose and had significantly higher levels of serum P, non-esterified fatty acids (NEFA) and β-hydroxybutyrate (BHBA) than their healthy counterparts on calving day. However, the serum calcitonin and PTH concentrations were not significantly different between the two groups. These data demonstrated that the concentrations of macrominerals and major calcium regulating hormones of cows change dramatically over the peripartum period. Furthermore, SCH was associated with a risk of the development of ketosis and fatty liver.

Ways of calcium reabsorption in the kidney

The role of the kidney in calcium homeostasis has been reshaped from a classic view in which the kidney was regulated by systemic calcitropic hormones such as vitamin D3 or parathyroid hormone to an organ actively taking part in the regulation of calcium handling. With the identification of the intrinsic renal calcium-sensing receptor feedback system, the regulation of paracellular calcium transport involving claudins, and new paracrine regulators such as klotho, the kidney has emerged as a crucial modulator not only of calciuria but also of calcium homeostasis. This review summarizes recent molecular and endocrine contributors to renal calcium handling and highlights the tight link between calcium and sodium reabsorption in the kidney.

Calcitropic Hormones and IGF-I Are Influenced by Dietary Protein

Elderly men and women with protein deficiencies have low levels of circulating IGF-I, and it is likely this contributes to reduced bone formation and increased bone resorption. We hypothesized that calcitropic hormones are involved in this effect and are affected by dietary protein. We therefore investigated the influence of a low-protein diet on the PTH-1,25-dihydroxyvitamin D3 [1,25(OH)2D3] axis and IGF-I in rats, using pamidronate to block resorption that normally contributes to mineral homeostasis. We fed 6-month-old Sprague Dawley female rats isocaloric diets containing 2.5% or 15% casein for 2 wk. Pamidronate was then administered sc (0.6 mg/kg/) for 5 d. Blood samples were collected at different time points. Serum 1,25(OH)2D3, IGF-I, PTH, calcium, and phosphorus were determined in all rats; vertebral bone strength and histomorphometric analysis were performed in rats subject to the longest low-protein diets. We found 2 wk of low protein increased PTH levels, decreased 1,25(OH)2D3, calcium, and IGF-I, suggesting that increased PTH compensates for low-protein-induced decreases in 1,25(OH)2D3. Pamidronate augmented the increased PTH after 8 wk of low protein and prevented the 1,25(OH)2D3 decrease. IGF-I remained low. Protein malnutrition induced decreases in relative bone volume and trabecular thickness, which was prevented by pamidronate. Maximal load was reduced by protein restriction, but rescued by pamidronate. In summary, the low protein diet resulted in hyperparathyroidism, a reduction in circulating levels of IGF-I, and reduced 1,25(OH)2D3 despite hyperparathyroidism. Blocking resorption resulted in further increases in PTH and improved microarchitecture and biomechanical properties, irrespective of vitamin D status or protein intake.