Pilot studies to demonstrate that intestinal mucosal afferent nerves are functionally linked to visceral adipose tissue.

Dietary capsaicin reduces rodent visceral fat weight. We tested the hypothesis that intact intestinal mucosal afferent nerve function is necessary for fat deposition in visceral adipose tissue sites. Rats were treated daily for 2 weeks with intragastric (chronic treatment) vehicle or capsaicin. Superior mesenteric artery blood flow and mesenteric and inguinal fat blood flow were measured before and after capsaicin was administered into the duodenum (acute treatment). Fat from all sites was dissected and weighed. Chronic capsaicin significantly attenuated acute capsaicin-induced mesenteric hyperemia but did not abolish the reflex wiping of the eye exposed to capsaicin, indicating that functional ablation was limited to the intestinal mucosal afferent nerves. The associated vasoconstriction in adipose tissue was inhibited at the visceral (mesenteric) site and maintained but attenuated at the subcutaneous (inguinal) site. The onset of vasoconstriction was instantaneous, indicating a reflex mechanism. There was a redistribution of fat from visceral to subcutaneous sites, reflected by a decrease and an increase in the percentage of body fat in the visceral and subcutaneous sites, respectively. These pilot studies reveal for the first time that normal intestinal mucosal afferent nerve function is necessary for the physiologic accumulation of fat in visceral adipose tissue sites.

The significance of carotid artery atheromas on panoramic radiographs in the diagnosis of occult metabolic syndrome.

OBJECTIVE: Metabolic syndrome (MetS), the co-occurrence of abdominal obesity, hypertriglyceridemia, reduced HDL cholesterol, hypertension, and insulin resistance promotes carotid atherosclerosis and stroke. The objective of this study was to determine if the presence of calcified atheromas detected on panoramic radiographs of individuals free of overt vascular disease may herald occult MetS. STUDY DESIGN: Ninety-four individuals (mean age 65.6 years) with a calcified atheroma detected by a VA dental clinic were evaluated. A like-aged group was used for comparative analysis. RESULTS: Fifteen percent of individuals (mean age 64 years) with an atheroma had occult MetS. Mean waist circumference was 116 cm, BMI 32.7 kg/m2, triglycerides 250 mg/dL, HDL cholesterol 35 mg/dL, blood pressure 147/87 mm Hg, and glucose 117 mg/dL. Only 6% of controls had occult MetS but this difference in prevalence was not proven to be statistically significant (P = .059). CONCLUSION: Some individuals with a calcified atheroma may have undiagnosed MetS and should be referred to their physician because aggressive management may preclude a stroke.

Impaired endothelial alpha-2 adrenergic receptor-mediated vascular relaxation in the fructose-fed rat.

To investigate the vascular endothelial dysfunction in the insulin resistance syndrome, muscarinic and alpha2-adrenergic mediated relaxations were studied in the fructose-fed rat. Male Sprague-Dawley rats were fed either fructose-rich chow (FFR, n=14) or normal chow (CNT, n=13) for 8 weeks. Systolic blood pressure (SBP) was measured by the tail-cuff method. A 3 mm segment of mesenteric artery was cannulated and pressurized, pretreated with prazosin (10(-6) mol/l) and propranolol (3x10(-6) mol/l), then pre-contracted with serotonin (10(-6) mol/l). Endothelium-dependent relaxation was induced by addition of acetylcholine (ACh, 10(-9)-10(-4) mol/l) or a selective alpha2-agonist, B-HT 920 (10(-9)-10(-5) mol/l), with or without the nitric oxide (NO) synthase inhibitor, L-NAME (10(-4) mol/l). SBP was significantly elevated in FFR but not in CNT. Plasma triglyceride in FFT (241+/-115 mg/dl) was significantly (p<0.01) higher than in CNT (84+/-34 mg/dl). Insulin and insulin/glucose ratio were higher but not significantly. Plasma glucose was not different between the two groups. In the dose-response curves to ACh, maximum relaxation and ED50 were similar between FFR and CNT. Moreover, L-NAME shifted the dose-response curves similarly to the right in both groups. Dose-response curves to B-HT 920, however, showed less relaxation in FFR than in CNT (p<0.05). B-HT 920-induced relaxations were mostly abolished by L-NAME. It is concluded that endothelial alpha2-adrenergic relaxation, predominantly mediated by NO, is likely more sensitive to the development of insulin resistance than muscarinic receptor relaxation in this 8-weeks FFR model. This early impairment of endothelial alpha2-adrenergic relaxation may contribute to the development of hypertension and insulin resistance in the FFR.