Early and longer term effects of gastric bypass surgery on tissue-specific insulin sensitivity and beta cell function in morbidly obese patients with and without type 2 diabetes

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PATIENTS WITH MIXED CRYOGLOBULINEMIA AND HCV INFECTION, IN PRESENCE OR ABSENCE OF AUTOIMMUNE THYROIDITIS, HAVE HIGH SERUM LEVELS OF (CXC MOTIF) LIGAND (CXCL)9 AND CXCL11 CHEMOKINES

No data are present in the literature regarding chemokine (CXC motif) ligand (CXCL)9 and CXCL11 circulating levels in cryoglobulinemia associated with hepatitis C (MC+HCV), in presence/absence of autoimmune thyroiditis (AT). Serum CXCL9 and CXCL11 have been measured in 38 MC+HCV patients without AT (MCo), 38 MC+HCV patients with AT (MC+AT), and in matched controls without (control 1) or with thyroiditis (control 2). Serum CXCL9 and CXCL11 were significantly higher: in control 2 than control 1 (p<0.05); in MCo than control 1 and control 2 (p<0.001, for both); in MC+AT than control 1 and control 2 (p<0.0001, for both), and than MCo (p=0.01, for both). Our study demonstrates markedly high serum levels of CXCL9 and CXCL11 in patients with MC+HCV compared to healthy controls; in MC+HCV patients increased CXCL9 and CXCL11 levels were significantly associated with the presence of AT. Moreover, a strong relation between circulating CXCL9 and CXCL11 in MC+HCV has been shown

LDL resistance to oxidation: Effects of lipid phenotype, autologous HDL and alanine

Background: Although LDL resistance to copper-induced oxidation is a time-honoured method, how it is modulated by the physiologic variability of lipid phenotype and what influences the protective action of homologous HDL and exogenous alanine is still unclear. Methods: In 159 subjects without severe dyslipidemias, LDL resistance to copper-induced oxidation (lag phase) was measured under standardised conditions, with alanine and with autologous HDL. Results: Lag phase was normally distributed and averaged 68 +/- 10 min (range: 40-105 min). Both VLDL-triglycerides (37 +/- 5, 52 +/- 7, 59 +/- 7, 53 +/- 5 mg/dl, p<0.05) and LDL-triglycerides (27 +/- 2, 27 +/- 1, 30 +/- 2, 35 +/- 3 mg/dl, p<0.01) increased across quartiles of lag phase. The relative LDL enrichment in triglycerides (triglycerides percent or triglycerides/cholesterol ratio) was strongly related to lag phase (r=0.29 and r=0.31, p<0.0005 for both) independently of age, gender, BMI, and presence of diabetes or hypertension. The protective effect of HDL was variable (+42 +/- 18 min) and largely dependent on the capacity of HDL to resist oxidation (r=0.69,p<0.0001). Alanine induced a rather constant lag phase prolongation (+32 +/- 7 min) that was weakly related only to baseline lag phase (r=0.17,p<0.05). Conclusions: Relative triglyceride abundance protects LDL from ex-vivo oxidation, HDL particles protect LDL mainly through substrate dilution and alanine probably through a direct anti-oxidant effect. (c) 2007 Elsevier B.V. All rights reserved

FOREARM METABOLIC RESPONSE TO ADENOSINE-INDUCED VASODILATION IN ESSENTIAL-HYPERTENSION

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A Protein/Lipid Preload Attenuates Glucose-Induced Endothelial Dysfunction in Individuals with Abnormal Glucose Tolerance

Postprandial hyperglycemia interferes with vascular reactivity and is a strong predictor of cardiovascular disease. Macronutrient preloads reduce postprandial hyperglycemia in subjects with impaired glucose tolerance (IGT) or type 2 diabetes (T2D), but the effect on endothelial function is unknown. Therefore, we examined whether a protein/lipid preload can attenuate postprandial endothelial dysfunction by lowering plasma glucose responses in subjects with IGT/T2D. Endothelial function was assessed by the reactive hyperemia index (RHI) at fasting, 60 min and 120 min during two 75 g oral glucose tolerance tests (OGTTs) preceded by either water or a macronutrient preload (i.e., egg and parmesan cheese) in 22 volunteers with IGT/T2D. Plasma glucose, insulin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), glucagon, free fatty acids, and amino acids were measured through each test. RHI negatively correlated with fasting plasma glucose. During the control OGTT, RHI decreased by 9% and its deterioration was associated with the rise in plasma glucose. The macronutrient preload attenuated the decline in RHI and markedly reduced postprandial glycemia. The beneficial effect of the macronutrient preload on RHI was proportional to the improvement in glucose tolerance and was associated with the increase in plasma GLP-1 and arginine levels. In conclusion, a protein/lipid macronutrient preload attenuates glucose-induced endothelial dysfunction in individuals with IGT/T2D by lowering plasma glucose excursions and by increasing GLP-1 and arginine levels, which are known regulators of the nitric oxide vasodilator system

Daylong pituitary hormones in morbid obesity: effects of bariatric surgery

Moderate obesity is known to be associated with multiple endocrine abnormalities. Less information is available on the hormonal status of patients with morbid obesity and on the effects of major weight loss. We studied 16 severely obese (BMI 40.6-69.9 kg/m(2)) nondiabetic patients and 7 nonobese (BMI range 24.6-27.7 kg/m(2)), sex- and age-matched healthy volunteers. During 24 h in a metabolic ward, four meals were administered and hourly blood samples were drawn from a central venous catheter for the measurement of glucose, insulin, leptin, thyrotropic hormone (TSH), growth hormone (GH) and prolactin. Insulin sensitivity was measured by a euglycaemic hyperinsulinaemic clamp. Studies were repeated 6 months after biliopancreatic diversion, a mainly malabsorptive surgical approach, which caused an average weight loss of 35 +/- 4 kg ( or 26 +/- 2% of initial weight). Compared with controls, patients were hyperinsulinaemic ( 290 +/- 31 vs 88 +/- 4 pmol l(-1), P = 0.0002), insulin resistant (23.5 +/- 2.8 vs 52.9 +/- 4.9 mmol min(-1) kg FFM(-1), P = 0.0006) and hyperleptinaemic (52.5 +/- 5.8 vs 10.9 +/- 3 ng ml(-1), P = 0.0002). Plasma TSH levels were increased throughout the day-night cycle (averaging 2.02 +/- 0.18 vs 1.09 +/- 0.19 mu U ml(-1) of controls, P = 0.01), whereas serum GH levels were suppressed (0.46 +/- 0.10 vs 3.01 +/- 1.15, P = 0.002). Following surgery, the hyperinsulinaemia and insulin resistance were fully normalized; in concomitance with a major drop in leptin levels (to 14.4 +/- 2.7 ng ml(-1), P = 0.02), TSH decreased and GH increased to near-normal levels. In the whole dataset, mean 24-h leptin levels were directly related to mean 24-h TSH levels after controlling for confounders this relationship was lost only after adjusting for fat mass. We conclude that in morbid obesity leptin is a determinant of changes in pituitary function