Comparison of clinical outcomes following early rehabilitation in 3 cases of nephrotic syndrome with different treatment courses.

There have been few published reports regarding rehabilitation for nephrotic syndrome. We compared the clinical outcomes of three cases of nephrotic syndrome with different treatment courses during 5 weeks of early rehabilitation.We report on three cases of nephrotic syndrome. Case 1 was a 67-year-old male who showed good progress after steroid treatment. Quadriceps torque and exercise capacity were increased after intervention. Case 2, a 78-year-old male, demonstrated resistance to steroid treatment. Quadriceps torque was decreased and exercise capacity was increased after intervention. Case 3 was an 83-year-old male who received nutrition therapy and diuretics without steroid treatment. Quadriceps torque and exercise capacity were decreased post-intervention.Early rehabilitation should be considered even if the steroid treatment course is different; furthermore, it is necessary to carefully consider the optimal exercise load in patients with nephrotic syndrome for whom regardless of whether or not steroid treatment is used.

Hypothalamic AMP-Activated Protein Kinase Regulates Biphasic Insulin Secretion from Pancreatic ß Cells during Fasting and in Type 2 Diabetes.

Glucose-stimulated insulin secretion (GSIS) by pancreatic ß cells is biphasic. However, the physiological significance of biphasic GSIS and its relationship to diabetes are not yet fully understood. This study demonstrated that impaired first-phase GSIS follows fasting, leading to increased blood glucose levels and brain glucose distribution in humans. Animal experiments to determine a possible network between the brain and ß cells revealed that fasting-dependent hyperactivation of AMP-activated protein kinase in the hypothalamus inhibited first-phase GSIS by stimulating the ß-adrenergic pancreatic nerve. Furthermore, abnormal excitability of this brain-ß cell neural axis was involved in diabetes-related impairment of first-phase GSIS in diabetic animals. Finally, pancreatic denervation improved first-phase GSIS and glucose tolerance and ameliorated severe diabetes by preventing ß cell loss in diabetic animals. These results indicate that impaired first-phase GSIS is critical for brain distribution of dietary glucose after fasting. Furthermore, ß cells in individuals with diabetes mistakenly sense that they are under conditions that mimic prolonged fasting. The present study provides additional insight into both ß cell physiology and the pathogenesis of ß cell dysfunction in type 2 diabetes.