Peripheral glucose metabolism in patients with chronic renal failure

The present study was designed to determine the effect of chronic renal failure on forearm muscle glucose uptake and oxidation during the postabsorptive state and after an oral glucose challenge. Twelve normal subjects and sixteen patients with chronic renal failure were studied after an overnight fast (12-14h) and for 3h after the ingestion of 75g glucose. Peripheral glucose metabolism was analyzed by the forearm technique to estimate muscle exchange of substrate combined with indirect calorimetry. decreased forearm glucose uptake was observed in uremic patients compared to normal subjects (9l.5 ñ 11,4 vs 154.8 ñ 7.8mg 100 ml forearm -1 3h-1) with diminished nonoxidative glucose metabolism (69.4 ñ 12.1 vs 117.2 ñ 12.8mg 100 ml forearm-1 3h-1). Muscle glucose oxidation did not difer significantly between groups. Both serum free fatty acid levels and lipid oxidation rates were similar in the normal subjects and the uremic patients, and declined in a similar fashion after glucose ingestion. Basal serum insulin levels did not differ significantly between normal and uremic patients, whereas the insulinemic response to glucose load was greater among the patients with chronic renal failure. These data show that resistance occurring in patients with chronic renal failure is accompanied by impaired muscle glucose uptake and nonoxidative glucose metabolism

Serum levels of tumor necrosis factor in insulin-dependent diabetic patients

We determined the serum concentrations of tumor necrosis factor (TNF) in 15 nondiabetic healthy subjects and in 36 insulin-dependent (Type I) diabetic outpatients. The mean (ñ SD) annual fasting plasma glucose, urine glucose and HbA, levels of the diabetic group were 179 ñ 71 mg/dl, 13.0 ñ 13.2 g/day and 12.3 ñ 1.3%, respectively. The mean serum TNF concentration measured by immunoradiometric assay of the diabetic group *8.6 ñ 1.9 pg/ml) was significantly higher than healthy controls (6.9 ñ 0.9 pg/ml). Within the diabetic group, there was no correlation between serum TNF levels and either duration of diabetes or indices of metabolic control. However, serum TNF levels progressively increased from the well to the poorly controlled diabetic groups: 8.1 ñ 1.5 (G), 8.2 ñ 1.4 %): 8.4 ñ 2.4, 11.7 ñ 1.8 and 14.6 ñ 1.2, respectively. Serum TNF levels of the diabetic patients with chronic complications (N=7, 9.5 ñ 2.3 pg/ml) and without complications (N=29, 8.4 ñ 1.7 pg/ml) were statistically higher than control subjects. The progressive increase of the serum TNF levels from the the poorly controlled diabetic groups suggest a relationship between levels of this cytokine glycosylation

Effect of oral glucose on peripheral muscle fuel metabolism in fasted men

1. The metabolic adaptations of peripheral muscle during a 5-day "modified" fast (daily oral intake of 200 g of glucose)were studied in 12 normal males. the volunteers were studied nintially after receiving a balanced 2,400-Kcal diet for at least 3 days (S1) and then after 5 days of modified fast (S2). The forearm muscle exchange of energy substrate (glucose) and the carbohydrate and lipid oxidation rates in muscle were measured during the postabsorptive state (S1) and after an oral glucose challenge (S2). 2. Glucose intolerance was not observed in either situation. Arterial glucose levels increased from a basal value of 83 mg/100 to 171 mg/100ml in S1 and to 187 mg/100ml in S2 at 30 and 60 min, respectively, and returned to basal values at 180 min in both studies. Increased forearm glucose uptake was observed in S2 compared do S1(131.7 ñ 17.1 vs 92.6 ñ 12.0 mg 100 ml forearm **-1 h**1), with decreased glucose oxidation (23.8 ñ 3.7 vs 30.4 ñ 4.7 mg 100 ml forearm**-1 3h**-1) and increased glucose storage (9.80 ñ 16.6 vs 62.2 ñ 10.8 mg 100 ml forearm**-1 3h**-1) as muscle glycogen. 3. Basal serum free fatty acid (FFA) levels were significantly more elevated in S2 than S1 (1030 ñ 95 vs 657 ñ 59 micron mol/l; P < 0.05zz0 but were markedly reduced by glucose ingestion in both studies (352 ñ 33 (S2) vs 364 ñ 30 (S1) micron mol/l at 120 min). Basal FFA oxidation was similar in both studies (0.091 ñ 0.015 (S1) vs 0.105 ñ 0.019 (S2) mg 100 ml forearm **-1) and decreased significantly 3 after glucose ingestion only in S1 (0.030 ñ 0.010 (S1) vs 0.078 ñ 0.020 (S2) mg 100 ml forearm[[-1 min**-1; P < 0.05). 4. The insilun response to oral glucose was similar in both studies (11,060 ñ 899(S1) vs 11,078 ñ 918(S2) micronU ml**-1 3h**-1, but tjhe peak concentration occurred later (60 min (S2) vs 30 min (S1) and basal levels were significantly lowe in S2 compared to S1 (9.2) ñ 1.7 vs 11.1 ñ 1.5 micronU/ml; P < 0.05)...