Introduction: Glucagon-like peptide-1 (GLP-1) is an incretin hormone with multiple actions in addition to control of glucose homeostasis. GLP-1 is known to cause natriuresis in humans, but the effects on basic renal physiology are still partly unknown. Subjects and Methods: Twelve healthy young males were examined in a randomized, controlled, double-blinded, single-day, crossover trial to evaluate the effects of 2 hours GLP-1 infusion on kidney functions. Glomerular filtration rate (GFR) and renal plasma flow (RPF) were assessed with 51Cr-EDTA and 123I-hippuran, respectively, using a constant infusion renal clearance technique based on timed urine sampling. Results: GLP-1 had no significant effect on either GFR [+1.9%, 95% confidence interval (−0.8; 4.6%)] or RPF [+2.4%, 95% confidence interval (−3.6; 8.8%)]. Fractional urine excretion of lithium increased 9% (P = .013) and renal sodium clearance increased 40% (P = .007). Angiotensin II decreased 19% (P = .003), whereas renin, aldosterone, and the urinary...

Glucagon-like peptide-1 (GLP-1): effect on kidney hemodynamics and renin-angiotensin-aldosterone system in healthy men.

Vibrio cholerae serogroup O139 Bengal, a novel strain with epidemic potential, completely displaced V. cholerae serogroup 01 in Calcutta in January 1993, which was followed by an epidemic caused by V. cholerae O139 in March-May 1993. From November 1992 to July 1993, 95.6% of 916 V. cholerae isolates submitted to the National Institute of Cholera and Enteric Diseases from 28 locations in India were confirmed as serogroup O139. As of July 1993, V. cholerae O139 had been isolated from 13 Indian states and a union territory, and large outbreaks of cholera caused by the O139 serogroup had occurred in several cities. The extent of spread of V. cholerae O139 Bengal in India and its ability to swiftly disseminate leaves little doubt that this is the beginning of the eighth pandemic of cholera.

Spread of Vibrio cholerae 0139 Bengal in India

The classical concept of the renin–angiotensin system (RAS) is that of a blood-borne cascade, whose final and bioactive product, angiotensin II, plays an important endocrine role in the maintenance of blood pressure and electrolyte as well as fluid balance. In addition to this circulating RAS, there are an increasing number of studies to suggest the existence of a local angiotensin-generating system in several tissues. The so-called tissue RAS can act locally as a paracrine and/or autocrine factor in meeting specific needs for individual tissues and it can operate, in whole or in part, independently of the circulating counterpart. Recent studies on the expression and localization of key RAS components, particularly angiotensinogen and renin, have provided solid evidence for the existence of an intrinsic, angiotensin-generating system in the pancreas. The tissue RAS has a potential role in finely regulating exocrine and endocrine functions of the pancreas such as ductal anion secretion and islet hormonal secretion. Some of these effects may be exerted via the markedly vasoconstrictive effects of RAS. Of particular interest in this context are the recent epidemiological data showing that administration of angiotensin-converting enzyme inhibitors appears to be protective against the development of diabetes in hypertensive patients. Moreover, the upregulation of pancreatic RAS has been shown to occur during chronic hypoxia. The significance of changes in pancreatic RAS could have a potential role in acute pancreatitis, islet transplantation and in different shock states, by causing a further decrease of blood perfusion in the pancreas.

/pdf/tissue-renin-angiotensin-system-its-expression-localization-ymi3q81gia.pdf

Tissue renin-angiotensin system: its expression, localization, regulation and potential role in the pancreas

People with hypertension have a high prevalence of insulin resistance and are at relatively high risk of developing type 2 diabetes mellitus. It is becoming increasingly evident that antihypertensive agents have disparate metabolic effects. For example, recent clinical trials indicate that agents that interrupt the renin-angiotensin axis reduce the risk of developing diabetes compared with other classes of antihypertensive agents. Blockade of the effects of angiotensin II might improve blood flow to insulin-sensitive tissues. Furthermore, interruption of the renin-angiotensin system might provide metabolic benefit through such mechanisms as reduced oxidative stress and restored nitric oxide production, which could lead to improved insulin signaling. Alternatively, collective trials suggest that both diuretics and β-blockers accelerate the appearance of new-onset type 2 diabetes mellitus in patients with hypertension. Therefore, the risk of new-onset diabetes-associated cardiovascular risks should be factored into future treatment recommendations for patients who require antihypertensive therapy. This will become even more important as the number of insulin-resistant patients with hypertension increases in parallel with the steady growth in the number of sedentary, obese, and aged persons in our population.

Effect of antihypertensive agents on the development of type 2 diabetes mellitus.

2 Abstract: An experiment was carried out during 2011 and 2012 seasons to study the effect of foliar application by using some growth regulators (paclobutrazol at 300 ppm, gibberellic acid (GA ) at 80 ppm and NAA at 3 40 ppm) and mineral nutrients (3% Ca as calcium chloride (CaCl ), 0.3 % boron as boric acid and 0.3 % Zn as zinc 2 sulphate (ZnSO ) after two and eight weeks from full bloom on yield, fruit cracking% and quality in pomegranate 4 cultivar 'Manfalouty'. The extent of fruit cracking was reduced significantly with application of 300 ppm pacloputrazol, while grain %, fruit juice %, TSS % and acidity % were increased. Yield and fruit weight were increased with applying pacloputrazol or by using (3 % Ca + 0.3 % B + 0.3 % Zn). Application of 40 ppm NAA and 80 ppm GA significantly increased fruit length and fruit diameter. Application of 80 ppm GA significantly 33 increased total anthocyanin %, while tannins % was not affected by other two growth regulators.

/pdf/cracking-and-fruit-quality-of-pomegranate-punica-granatum-l-1hzn82scyn.pdf

Cracking and Fruit Quality of Pomegranate (Punica granatum L.) As Affected by Pre-Harvest Sprays of Some Growth Regulators and Mineral Nutrients

Angiotensin II (Ang II) modulates the tissue response to insulin (insulin sensitivity), but the effect of Ang II on the secretion of insulin has not been investigated thus far. Nineteen healthy volunteers (17 male; mean age, 26±1 years) were studied. In a double-blind, randomized, placebo-controlled study, seven volunteers were allocated on three occasions in random order after an overnight fast to three interventions: (1) solvent (placebo) infusion; (2) infusion of 1.0 ng Ang II · kg−1 · min−1 (subpressor dose); and (3) infusion of 5.0 ng Ang II · kg−1 · min−1 (pressor dose). Frequent blood samples (each minute) were obtained for estimation of plasma insulin concentrations over a period of 120 minutes to assess basal and pulsatile insulin secretion. In an ancillary study, plasma glucose and insulin levels were measured after an oral glucose tolerance test while solvent (placebo) or Ang II was infused in 12 fasting healthy volunteers. Plasma insulin concentrations were measured immunoenzymatically (enzyme-linked immunosorbent assay). Insulin secretion pulses were analyzed with the deconvolution technique, and the regularity of insulin secretion was analyzed with the approximate entropy technique. Plasma insulin half-life was assessed using the hyperinsulinemic euglycemic clamp method. The pressor dose of Ang II reduced total, basal, and pulsatile insulin secretion, and this effect was highly significant ( P <.01). The subpressor dose tended to suppress insulin secretion. The burst frequency (number of peaks) and the regularity of insulin secretion were not affected by administration of Ang II. After the oral glucose load, the insulinemic response was significantly lower and plasma glucose concentrations were significantly higher with infusion of Ang II compared with placebo. Ang II affects both the basal (nonpulsatile) and the pulsatile component of spontaneous insulin secretion and the glucose-stimulated insulin secretion in humans. This observation is of potential interest with respect to the interaction of Ang II and insulin, eg, in the genesis of hyperinsulinemia and hypertension.

Angiotensin II Affects Basal, Pulsatile, and Glucose-Stimulated Insulin Secretion in Humans

chondrocytes in vitro

Urinary secretory IgA (slgA) was measured using a specific ELISA wlth Insolublllzed antl-lgA and enzyme-llnked antlsecretory component. Thls test was applled to unprocessed urine from healthy chlldren and from chlldren with urinary tract Infectlon. Normal range was a functlon of age. In 175 healthy chlldren the excretion rate of slgA was low In Infants younger than 6 months but was constant between ages 6 months to 15 years (median 0.69 rag/gin creatlnlne, range 0.15 to 3.4 mg/gm creatlnlne), whereas slgA concentratlon (mllllgrams per llter of urine) Increased contlnuously wlth age. No sex dlfference was noted. There were no slgnlficant clrcadlan changes or day-to-day variablllty. Thldy glrls, age I to 16 years, were examined; they had a history of recurrent symptomatlc eplsodes of urlnary tract Infectlon but had anatomlcally normal tracts and no symptoms, and no bacterlurla at the tlme of study, slgA excretlon rate was slgnlficantly lower (0.45 mg/gm, creatlnlne, 0.08 to 0.75 mg/gm creatlnlne) than In controls. In contrast, 11 girls examined at the time of symptomatlc urinary tract Infectlons, and who had normal urinary tracts, had slgnlficantly (P <0.01) higher slgA excretlon rates (1.4 mg/gm creatlnlne, 0.8 to 3.4 mg/gm creatlnlne) than those In elther control subjects or glris wlthout symptoms at the tlme of study. Urinary slgA excretlon rates were highest (2.0 mg/gm creatlnlne, 0.44 to 3.69 rag/gin creatlnlne) In chlldren wlth symptomatlc urinary tract Infectlons who had an abnormal urinary tract. We conclude that low urinary slgA values may be a marker for recurrent symptomatlc bacterlurla in glris wlth normal urinary tracts. (J PEDIATR 1986;109:416-421)

Urinary slgA in children with urinary tract infection

Secondary (renal) hyperparathyroidism ― Diagnosis and medical management

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Angiotensin II Affects Basal, Pulsatile, and Glucose-Stimulated Insulin Secretion in Humans

chondrocytes in vitro

Urinary slgA in children with urinary tract infection

Secondary (renal) hyperparathyroidism ― Diagnosis and medical management