Insulin Prevents Hyperfiltration and Proteinuria but Not Glomerular Hypertrophy and Increases Mesangial Matrix Expansion in Diabetic Rats.

Objective: The aim of this work was to study the effect of 7 days of strict glycemic control with insulin on glomerular function and structure in streptozotocin (STZ)-diabetic rats.

Materials And Methods: Three groups of adult male Fischer rats were studied: controls (n = 15), diabetics (n = 15), and insulin-treated diabetics (n = 15). Diabetes was induced by treating the rats with STZ (55 mg/kg i.

Phlorizin prevents glomerular hyperfiltration but not hypertrophy in diabetic rats.

The relationships of renal and glomerular hypertrophies to development of hyperfiltration and proteinuria early in streptozotocin-induced diabetes were explored. Control, diabetic, phlorizin-treated controls, and diabetic male Fischer rats were used. Phlorizin (an Na+-glucose cotransport inhibitor) was given at a dose sufficient to normalize blood glucose.

Pulmonary ventilatory functions and obesity in Kuwait.

Objective: To study the relationship between obesity and pulmonary ventilatory functions in Kuwaiti adults.

Subjects And Methods: A total of 200 male and 180 female Kuwaiti adults aged 20-65 years were investigated in six medical centers from April 2004 to March 2006. Parameters measured included forced expiratory volume in 1 s (FEV(1)), forced vital capacity (FVC), FEV(1) as a percentage of FVC (FEV%); body mass index (BMI in kg/m(2)) and waist-to-hip ratio (W/H).

Interactions of the growth-related, type IIc renal sodium/phosphate cotransporter with PDZ proteins.

Despite similar molecular structures, the growth-related sodium/phosphate cotransporter NaPiIIc is regulated differently than the main NaPiIIa phosphate transporter. Using two-hybrid systems and immunoprecipitation, we identified several proteins that interact with NaPiIIc that might account for this differential regulation. NaPiIIc interacted with the PDZ domain-containing sodium-hydrogen exchange-regulating factor (NHERF) 1 and NHERF3 through novel binding motifs in its C terminus.

Cell-matrix interactions modulate transepithelial phosphate transport in P(i)-deprived OK cells.

In opossum kidney (OK) cells as well as in kidney proximal tubules, P(i) depletion increases apical (A) and basolateral (B) Na(+)-dependent P(i) cell influxes. In OK cells' monolayers in contrast to proximal tubules, there is no increase in transepithelial P(i) transport. This limitation may be due to altered cell-matrix interactions.