Search

To study anorexia in chronic renal failure (CRF) patients, we measured appetite-related hormones in seven CRF patients and four controls. Plasma concentrations and fractional changes from baseline (values from day 1, 0800) are listed as control vs. CRF (means [+ or -] SE). Leptin, although higher in CRF (5.6 [+ or -] 1.7 and 34 [+ or -] 17 ng/ml), was suppressed after fasting', decrements were -51 [+ or -] 9 and -55 [+ or -] 8%. Nocturnal surge present during feeding was abolished upon fasting in both groups. Neuropeptide Y (NPY) was elevated in CRF (72 [+ or -] 12 vs. 304 [+ or -] 28 pg/ml, P = 0.0002). NPY rhythm, reciprocal to that of leptin, was muted in CRF. Basal cortisol was similar in both groups (17 [+ or -] 3 and 17 [+ or -] 2 [micro]g/dl). In the controls, cortisol peaked in the morning and declined in the evening. CRF showed blunted cortisol suppression. Decrements were -61 [+ or -] 3 and -20 [+ or -] 9% at 1800 on day 1 (P = 0.008) and -61 [+ or -] 8 and -26 [+ or -] 8% at 2000 on day 2 (P = 0.02). Basal ACTH (25 [+ or -] 5 and 54 [+ or -] 16 pg/ml) as well as diurnal pattern was not statistically different between the groups. Baseline insulin was 6 [+ or -] 1 and 20 [+ or -] 9 [micro]U/ml. During fasting, insulin was suppressed to -64 [+ or -] 10 and -51 [+ or -] 9%, respectively. Upon refeeding, increments were 277 [+ or -] 96 and 397 [+ or -] 75%. Thus, in our CRF patients, anorexia was not due to excess leptin or deficient NPY. Impaired cortisol suppression should favor eating. Insulin suppression during fasting and secretion after feeding should enhance both eating and anabolism. The constant high NPY suggests increased tonic hypersecretion. hormones; appetite; uremia

Increases in leptin levels, sympathetic drive, and weight gain in obstructive sleep apnea. Am J Physiol Heart Circ Physiol 279: H234-H237, 2000.--Patients with obstructive sleep apnea (OSA) are frequently obese and are predisposed to weight gain. They also have heightened sympathetic drive. We reasoned that noradrenergic activation of [[Beta].sub.3]-receptors on adipocytes would inhibit leptin production, predisposing to obesity in sleep apnea. We therefore tested the hypothesis that obesity and predisposition to weight gain in OSA are associated with low levels of plasma leptin. We prospectively studied 32 male patients (43 [+ or -] 2 yr) with OSA who were newly diagnosed and never treated and who were free of any other diseases. Control measurements were obtained from 32 similarly obese closely matched male subjects (38 [+ or -] 2 yr). Leptin levels were 13.7 [+ or -] 1.3 and 9.2 [+ or -] 1.2 ng/ml in patients with OSA and controls, respectively (P = 0.02). Weight gain over the year before diagnosis was 5.2 [+ or -] 1.7 and 0.5 [+ or -] 0.9 kg in sleep apnea patients and similarly obese control subjects, respectively (P = 0.04). Muscle sympathetic activity was 46 [+ or -] 4 and 30 [+ or -] 4 bursts/min in patients with OSA (n = 16) and control subjects (n = 18), respectively (P = 0.01). Plasma leptin levels are elevated in newly diagnosed otherwise healthy patients with untreated sleep apnea beyond the levels seen in similarly obese control subjects without sleep apnea. Higher leptin levels in OSA, independent of body fat content, suggest that OSA is associated with resistance to the weight-reducing effects of leptin. obesity; heart rate; sympathetic nervous system