Association between obstructive sleep apnea syndrome and bone mineral density in adult orthodontic populations.

OBJECTIVE: To determine the association between obstructive sleep apnea syndrome (OSAS) and predicted bone mineral density (BMD) in adults presenting for orthodontic treatment. METHODS: This retrospective cross-sectional study included 38 adults divided into OSAS and non-OSAS groups. Using pre-treatment CBCT images, radiographic density (RD) of left and right lateral regions of the 1st cervical vertebrae and dens of the 2nd cervical vertebrae were measured as an indicator for BMD. RESULTS: When controlling for age, sex, and BMI, the mean RD was significantly lower in the OSAS group compared to the non-OSAS group (left CV1: 36.69 ± 84.50 vs. 81.67 ± 93.25 Hounsfield Units [HU], respectively, p = 0.031; right CV1: 30.59 ± 81.18 vs. 74.26 ± 91.81 HU, p = 0.045; dens: 159.25 ± 115.96 vs. 223.94 ± 106.09 HU, p = 0.038). CONCLUSION: Adults with OSAS have lower values for predicted BMD than those without OSAS.

Resveratrol activates duodenal Sirt1 to reverse insulin resistance in rats through a neuronal network.

Resveratrol improves insulin sensitivity and lowers hepatic glucose production (HGP) in rat models of obesity and diabetes, but the underlying mechanisms for these antidiabetic effects remain elusive. One process that is considered a key feature of resveratrol action is the activation of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase sirtuin 1 (SIRT1) in various tissues. However, the low bioavailability of resveratrol raises questions about whether the antidiabetic effects of oral resveratrol can act directly on these tissues. We show here that acute intraduodenal infusion of resveratrol reversed a 3 d high fat diet (HFD)-induced reduction in duodenal-mucosal Sirt1 protein levels while also enhancing insulin sensitivity and lowering HGP. Further, we found that duodenum-specific knockdown of Sirt1 expression for 14 d was sufficient to induce hepatic insulin resistance in rats fed normal chow. We also found that the glucoregulatory role of duodenally acting resveratrol required activation of Sirt1 and AMP-activated protein kinase (Ampk) in this tissue to initiate a gut-brain-liver neuronal axis that improved hypothalamic insulin sensitivity and in turn, reduced HGP. In addition to the effects of duodenally acting resveratrol in an acute 3 d HFD-fed model of insulin resistance, we also found that short-term infusion of resveratrol into the duodenum lowered HGP in two other rat models of insulin resistance--a 28 d HFD-induced model of obesity and a nicotinamide (NA)-streptozotocin (STZ)-HFD-induced model of mild type 2 diabetes. Together, these studies highlight the therapeutic relevance of targeting duodenal SIRT1 to reverse insulin resistance and improve glucose homeostasis in obesity and diabetes.