Both apelin and asymetric dymethyl arginine (ADMA) regulate blood pressures. Low apelin and high ADMA levels have been reported in several cardiometabolic disorders. However, there is no data about ADMA and apelin levels in essential hypertension and any relationship between them. We investigated a group of newly diagnosed and untreated 30 young hypertensive men and 30 healthy controls. Apelin levels were significantly lower and the ADMA levels were significantly higher in the patients (p = 0.04 for both). Both ADMA and apelin were related to the systolic blood pressures (SBP) (beta = -0.393, p = 0.003; beta = 0.285, p = 0.03, respectively). Future studies are necessary in order to clearly define the role of ADMA and apelin in the pathogenesis of essential hypertension.

Recent studies ascribe a major role to pancreatic ␤-cell loss in type 2 diabetes. We investigated the dynamics of ␤-cell mass during diabetes evolution in Psammomys obesus, a model for nutrition-dependent type 2 diabetes, focusing on the very early and the advanced stages of the disease. P. obesus fed a high-calorie diet for 26 days developed severe hyperglycemia, ␤-cell degranulation, and markedly reduced pancreatic insulin content. Reducing calories for 7 days induced normoglycemia in 90% of the animals, restoring ␤-cell granulation and insulin content. To dissociate effects of diet from blood glucose reduction, diabetic animals received phlorizin for 2 days, which normalized glycemia and increased the pancreatic insulin reserve to 50% of control, despite a calorie-rich diet. During diabetes progression, ␤-cell mass decreased initially but recovered spontaneously to control levels, despite persistent hyperglycemia. Strikingly, however, ␤-cell mass did not correlate with degree of hyperglycemia or pancreatic insulin content. We conclude that reduced insulin reserve is the main cause of diabetes progression, whereas irreversible ␤-cell mass reduction is a late event in P. obesus. The rapid recovery of the pancreas by phlorizin-induced normoglycemia implies a causal relationship between hyperglycemia and islet dysfunction. Similar mechanisms could be operative during the evolution of type 2 diabetes in humans. Diabetes 54:138 -145, 2005 P ancreatic insulin reserve is an important parameter of islet function, with tight coupling between insulin secretion and production being necessary for the adequate functioning of the ␤-cell (rev. in 1). Insulin store size is determined by the balance between the rates of insulin biosynthesis and secretion as well as by the number and volume of the ␤-cells, i.e., the ␤-cell mass. In the adult, ␤-cell mass varies to adapt insulin secretion to long-term changes in insulin demand. This has been demonstrated repeatedly under physiological as well as pathological conditions of insulin resistance (rev. in 2). Although mainly demonstrated in rodents, this also seems to be the case in obese humans (3,4). The deterioration of the metabolic state in type 2 diabetes results mainly from progressive ␤-cell failure (5,6), hence the importance of determining whether functional ␤-cell mass is reduced in type 2 diabetes. This question remains controversial. Whereas some authors observed no change in ␤-cell mass (7-9), recent studies, using a large series of pancreata from patients with type 2 diabetes matched by appropriate control subjects, describe reduced relative ␤-cell volume or ␤-cell mass in humans with both impaired fasting glucose and established type 2 diabetes (4,10,11). The finding of reduced ␤-cell mass already in individuals with impaired fasting glucose has led to emphasizing its pathophysiological importance (9). In their recent evaluation of islets isolated from the pancreas of normal and type 2 diabetic cadaveric donors, Deng et al. (12) observed that in addition to a marked r...

The present study was conducted to evaluate the serum copper, zinc, magnesium, and selenium levels in patients with subclinical hypothyroidism in the iodine-rich region of Ankara, Turkey. The effects of hormone replacement therapy on these elements were also studied in these patients. Basal levels of selenium and iron in patients were significantly lower than control group (67.7 +/- 10.4 vs. 83.7 +/- 17.3 microg/dl, p = 0.02; 55.7 +/- 38 vs 275.7 +/- 24, P = 0.03 microg/dl). Serum magnesium levels were significantly higher in patient group (2.16 +/- 0.31 vs 1.95 +/- 0.13 mg/dl, P < 0.0001). There was a correlation between selenium levels with hsCRP (r = -0.408, p = 0.007). HsCRP levels in patients with selenium levels <80 microg/l (n = 31) was significantly higher than hsCRP levels in patients with selenium levels >80 microg/l (n = 12; 1.99 +/- 1.0; 1.02 +/- 0.9, p = 0.014). None of these biochemical risk factors and trace elements have changed after euthyroidism in patients with SH when compared to pretreatment levels. Selenium deficiency may contribute to cardiovascular disease risk in these patients.

Objective: The relationship between metabolic syndrome (MS) and hypogonadism has always been investigated in study groups confounded with aging, obesity or chronic metabolic disorders. So far, there has been no data about the presence of MS in young hypogonadal patients. Also, there is controversial data about the metabolic effects of testosterone replacement therapy. We investigated the frequency of MS in treatment-naïve, young men with congenital hypogonadal hypogonadism (CHH). We also searched for the effect of testosterone replacement on the metabolic profiles of this specific patient group. Design: Retrospective analysis. Methods: A total of 332 patients (age 21.68G2.09 years) were enrolled. The control group included 395 age-and body mass index (BMI)-matched healthy young men (age 21.39G1.49 years). Standard regimen of testosterone esters (250 mg/3 weeks) was given to 208 patients. Results: MS was more prevalent in CHH (P!0.001) according to healthy controls. The patients had higher arterial blood pressure, waist circumference (WC), triglyceride (P!0.001 for all), fasting glucose (PZ0.02), fasting insulin (PZ0.004), homeostatic model assessment of insulin resistance (HOMA-IR) (PZ0.002) and lower high density lipoprotein (HDL) cholesterol (P!0.001) levels. After 5.63G2.6 months of testosterone treatment, the BMI, WC (P!0.001 for both), systolic blood pressure (PZ0.002) and triglyceride level (PZ0.04) were increased and the total and HDL cholesterol levels were decreased (PZ0.02 and P!0.001 respectively). Conclusions: This study shows increased prevalence of MS and unfavorable effects of testosterone replacement in young patients with CHH. Long-term follow-up studies are warranted to investigate the cardiovascular safety of testosterone treatment in this specific population.

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