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The neotropical rodents Akodon cursor (2n = 14, 15, and 16) and A. montensis (2n = 24 and 25), two closely related and morphologically indistinguishable species, have been compared by G-banding and chromosome painting. In situ hybridization of a biotinylated DOP-PCR product obtained from a microdissected chromosome of A. cursor onto A. montensis chromosomes was performed in combination with localization of telomeric sequences using a (TTAGGG)n oligomer as a FISH probe. The results provide evidence of the complex chromosomal rearrangements suggested by GTG-banding analysis, indicating the origin of one A. cursor autosome from three different A. montensis autosomes. Furthermore, the complete cytogenetic homeology between the A. cursor and A. montensis karyotypes was determined, along with the occurrence of tandem fusions and pericentric inversions and the loss of telomeres, centromeres, and chromosome arms. Evidence for the ancestral origin of the A. cursor karyotype is also provided.

Leptin is usually associated to obesity, hyperinsulinemia, sodium metabolism and high blood pressure (BP). As leptin has a direct relationship to BMI, we compared in 25 hypertensive patients, age 43.9 ± 2.3 yrs, 8 white and 17 non-white, 8 male and 17 females, BMI 29.4 ± 1.1, the ratio leptin/BMI2 to the absolute values of leptin, in order to evaluate whether leptin/BMI2 is a more robust index of association of leptin with the variables of the metabolic syndrome. Serum levels of leptin and insulin were measured by RIA. Intraerythrocyte sodium content (NaIc) was determined by method of Cheng. Systolic, diastolic (DBP) and mean BP (MBP) were 149.7.4 ± 3.43, 93.9 ± 1.6 and 113.4 ± 1.8 mmHg, respectively. Fasting glucose, and insulin levels were 107.0 ± 4.1 mg/dl and 10. 2 ± 1.4 µU/ml, respectively. The 2 h area under the curve of insulin (AUC ins.) was 7168 ± 939 µU/ml/min. Serum concentration of leptin was 14.43 ± 1.84 ng/ml, and leptin/BMI 2 was 1.9 ± 0.21. Leptin/BMI 2 was associated to DBP (r = 0.41, p < 0.04), MBP (r=0.44, p < 0.03), NaIc (r=0.41, p < 0.05), age (r=0.43, p=0.03), AUC ins. (r=0.59 and p=0.002. Absolute levels of leptin did not correlate to the variables studied, except for the AUC ins. (r=0.40, p < 0.04). Our results suggest that leptin/BMI 2 is a simple and direct measure of leptin action in obese subjects. It is associated to hyperinsulinemia, BP and NaIc without the interference of the volume of adipose tissue.

Orlistat (OR) an inhibitor of pancreatic lipase has been suggested to act on body weight, but its consequence on the metabolic derangements of obesity are controversial. We investigate the effects of OR in 90 obese patients, 76 females and 14 males, 28 white and 62 non white, age 45.6 ± 2.6 years). OR was given during 3 months, 120mg tid, accompanied by a low fat caloric diet. Results before and after treatment were: weight 99.9 ± 2.0 vs 95.7 ± 1.9 kg; BMI 38.9 ± 0.7 vs 37.3 ± 0.7 kg/m 2 ; waist circumference 113.5 ±1.6 vs 108.3 ± 1.5 cm; waist to hip ratio (WHR) 0.92 ± 0.01 vs 0.91 ± 0.01; total chol 226.8 ± 5.2 vs 208.6 ± 5.0 mg/dl; LDL chol 151.6 ± 4.9 vs 140.1 ± 4.4mg/dl; triglycerides 137.4 ± 6.8 Vs 121.6 ± 6.5mg/dl, systolic (135.0 ± 2.3 vs 127.4 ±1.6 mmHg), diastolic (85.4 ±1.9 vs 79.0 ± 1.6 mmHg), and mean blood pressure 101.9 ± 1.9 vs 95.2 ± 1.5 mmHg, in all the comparisons p < 0.0003. Neither HDL (45.9 ± 1.2 vs 44.5 ± 1.0 mg/dl) nor fibrinogen (367.4 ± 10.6 vs 361.2 mg/dl) were different before and after orlistat intervention. Changes of glucose levels were correlated to weight loss (r = 0.28, p < 0.008), as well as to changes on waist (r=0.28, p=0.02). The association remained significant with waist circumference after correction for body weight. The changes of triglycerides were correlated both to waist circumference (r = 0.29, p = 0.006) and WHR (r = 0.23, p < 0.03), even when corrected by regression analysis for changes in body weight. Levels of blood pressure were not associated to changes of weight, as well as to changes of anthropometric indexes. Conclusions: In our obese patients, orlistat actuates on metabolism of lipid and glucose independently of its role on body weight reduction.

Previous studies have demonstrated the role of renal kallikrein (rKal), vasoactive kinins and nitric oxide (NO) in regulating the renal response to acute oral protein load (renal reserve, RR). The aim of this study was to evaluate the effects of protein load on renal hemodynamics of obese hypertensive patients and the possible participation of rKal and NO in this response. We studied 14 obese hypertensive patients, (BMI: 32.9 ± 1.1, age: 50.5 ± 0.9 yrs, SBP: 153.5 ± 2.8 mmHg, DBP:96.2 ± 2.2 mmHg, 5 males and 9 females). Hemodynamic and metabolic evaluations were conducted at basal condition and after protein challenge moment (1g/kg of weight). Glomerular filtration rate (GFR) was estimated by clearance of inulin, and renal plasma flow (RPF) was calculated by the clearance of 131 orthoiodohippurate. We measured the levels of plasmatic and urinary NO by the Griess reaction modified, and the urinary excretion of rKal by chromogenic substrate. The mean RR of the patients was 8.0 ± 1.1. After protein load there was a significant increase of urinary kal (0.12 ± 0.04 vs 0.29 ± 0.06 Kal/Cr, p = 0.002), plasma NO (22.1 ± 0.8 vs 25.8 ± 2.1 µM, p = 0.04), RPF (374.2 ± 25.5 vs 438.8 ± 27.2 ml/min, p = 0.02) and GFR (143.7 ± 7.8 vs 151.7 ± 7.0 ml/min, p = 0.0009), but no difference was observed in the urinary concentration of NO. We concluded that in obese hypertensive individuals, the vasodilator capacity of renal vasculature after protein load is preserved and may be mediated by renal kallikrein and NO.

During normal gestation nitric oxide (NO) has been recognized as a regulator of blood pressure (BP) through its effects on peripheral vascular resistance (PVR), counteracting the increase cardiac output (CO). We studied in 20 normal pregnant adolescents: PVR, CO, mean BP (MBP) using thoracic bioimpedance and serum levels of NO, throughout pregnancy: < 20 weeks, 20 to 30 weeks and > 30 weeks. 11 non pregnant adolescents were used as a control group (C). In pregnant adolescents the levels of NO were significantly higher at < 20 wks: 27.8 ± 1.6 µM (p = 0.03) and 20 to 30 wks of gestation, 29.6 ± 2.2 µM (p < 0.03), but not after 30 wks 26.3 ± 2.2, when compared to control individuals (22.3 ± 1.3 µ M). PVR decreased in the first two periods and increased in the latest (1102 ± 78 and 1016 ± 64 vs 1178 ± 66 dyne.sec.cm -5 , respectively, p < 0.05 comparing to values of C (1409 ± 85 dyne.sec.cm -5). The values of CO were different only at 20 to 30 wks when compared to C (9.4 ± 0.5 vs 6.8 ± 0.5 L/min, p < 0.05). BP did not differ between the two groups, in any period of gestation. We concluded that NO is an important mediator of the circulatory homeostasis during normal pregnancy.

Several studies have been documenting the relationship of sympathetic nervous activity (SNA), BP, and hyperinsulinemia in obese hypertensive patients. This study was conducted to evaluate the possible participation of leptin in these links. In 22 obese hypertensive patients (BMI=33.5 ± 1.1; MBP=124.5 ±1.6 mmHg; 58.8 ± 1.7 yrs) we evaluated, after 2 weeks of wash-out period, the arterial and venous levels of cathecolamine (measured by HPLC), serum leptin and insulin concentrations (by RIA), insulin resistance index (HOMA) and anthropometric measures. Concentrations of venous and arterial epinephrine (E) and nor-epinephrine (NE) were 45.7 ± 8.6 and 50.7 ± 10.4 µg/dl, 136.2 ± 27.0 and 142.9 ± 26.2 µg/dl, respectively. Levels of insulin, leptin, HOMA, glucose, and triglycerides were 29.1 ± 5.0 µU/ml, 25.9 ± 3.1 ng/ml, 7.7 ± 1.6, 103.5 ± 4.8mg/dl, 165.8 ± 19.3 µg/dl, respectively. Venous E was positively correlated to leptin: r = 0.63, p = 0.02 and to BMI: r = 0.54, p = 0.05. Arterial NE was associated to TG: r = 0.64, p < 0.05, fasting insulin r=0.63, p < 0.04, and to HOMA: r = 0.66, p < 0.04. We concluded that our obese hypertensive patients leptin may be another participant of the clustering components of Metabolic Syndrome.