Adequate vitamin D supplementation does not ameliorate bone loss following long limb-biliopancreatic diversion in morbidly obese women.

OBJECTIVES: The objective of this study is to investigate the effect of adequate vitamin D supplementation on bone mineral density (BMD) following long limb-biliopancreatic diversion (LL-BPD), a malabsorptive bariatric operation. BACKGROUND: Marked weight loss following bariatric surgery is associated with significant decrease in BMD, attributed to the weight loss and to nutritional, mineral, and vitamin D deficiencies resulting in secondary hyperparathyroidism. METHODS: Two groups, of 35 and 37 healthy, obese (BMI, 50.4 + 6.6 and 46.5 + 4.8 g/cm2), premenopausal, normally menstruating women underwent LL-BPD. Both groups received high-calcium diets, 600 IU of vitamin D, and 1000 mg elemental calcium daily, while group B received an extra dose of vitamin D (10,000 IU/day) during the first postoperative month, followed by dose adjustment in order to maintain 25OHD concentration higher than 30 µg/L. Areal BMD (aBMD) was measured at the lumbar spine preoperatively and 1 year postoperatively. RESULTS: One year postoperatively, BMI decreased by approximately 19 kg/m2 in both groups, while 25-OH-vitamin D levels did not change in group A (18.7 + 9.1 to 20.2 + 13.0 µg/L, (p = 0.57)) and increased in group B (15.58 ± 5.73 to 52.97 ± 15.46 µg/L, (p = < 0.001). PTH levels increased in group A (from 38.5 ± 12.2 to 51.2 ± 32.8 pg/ml) (p = 0.047) and decreased in group B (from 51.61 ± 18.7 to 45.1 ± 17.8 pg/ml) (p = 0.042). Lumbar spine aBMD decreased similarly in both groups (p = 0.311, for the comparison between groups) from 1.198 + 0.14 to 1.103 + 0.15 g/cm2 in group A (p < 0.001) and from 1.157 + 0.14 to 1.076 + 0.14 g/cm2 in group B (p < 0.001) and Z-score from 0.93 + 0.97 to 0.19 + 1.02, (p < 0.001) and from 1.15 + 1.29 to 0.419 + 1.28, (p < 0.001), respectively. CONCLUSIONS: LL-BPD leads to similar and significant bone mass reduction 1 year postoperatively, irrespective of adequate vitamin D replacement and in the absence of secondary hyperparathyroidism.

Mastic oil from Pistacia lentiscus var. chia inhibits growth and survival of human K562 leukemia cells and attenuates angiogenesis.

Mastic oil from Pistacia lentiscus var. chia, a natural plant extract traditionally used as a food additive, has been extensively studied for its antimicrobial activity attributed to the combination of its bioactive components. One of them, perillyl alcohol (POH), displays tumor chemopreventive, chemotherapeutic, and antiangiogenic properties. We investigated whether mastic oil would also suppress tumor cell growth and angiogenesis. We observed that mastic oil concentration and time dependently exerted an antiproliferative and proapoptotic effect on K562 human leukemia cells and inhibited the release of vascular endothelial growth factor (VEGF) from K562 and B16 mouse melanoma cells. Moreover, mastic oil caused a concentration-dependent inhibition of endothelial cell (EC) proliferation without affecting cell survival and a significant decrease of microvessel formation both in vitro and in vivo. Investigation of underlying mechanism(s) demonstrated that mastic oil reduced 1) in K562 cells the activation of extracellular signal-regulated kinases 1/2 (Erk1/2) known to control leukemia cell proliferation, survival, and VEGF secretion and 2) in EC the activation of RhoA, an essential regulator of neovessel organization. Overall, our results underscore that mastic oil, through its multiple effects on malignant cells and ECs, may be a useful natural dietary supplement for cancer prevention.