Abdominal adiposity and insulin resistance in obese men

We examined the independent relationships among various visceral and abdominal subcutaneous adipose tissue (AT) depots, glucose tolerance, and insulin sensitivity in 89 obese men. Measurements included an oral glucose tolerance test (OGTT), glucose disposal by euglycemic clamp, and abdominal and nonabdominal (e.g., peripheral) AT by magnetic resonance imaging (MRI). OGTT glucose and glucose disposal rates were related ( P < 0.05) to visceral AT ( r = 0.50 and −0.41, respectively). These observations remained significant ( P < 0.05) after control for nonabdominal and abdominal subcutaneous AT, and maximal O2 consumption (V˙o 2 max). Abdominal subcutaneous AT was not a significant correlate ( P > 0.05) of any metabolic variable after control for nonabdominal and visceral AT andV˙o 2 max. Division of abdominal subcutaneous AT into deep and superficial depots and visceral AT into intra- and extraperitoneal AT depots did not alter the observed relationships. Further analysis matched two groups of men for abdominal subcutaneous AT but also for low and high visceral AT. Men with high visceral AT had higher OGTT glucose values and lower glucose disposal rates compared with those with low visceral AT values ( P < 0.05). A similar analysis performed on two groups of men matched for visceral AT but also for high and low abdominal subcutaneous AT revealed no statistically different values for any metabolic variable ( P > 0.10). In conclusion, visceral AT alone is a strong correlate of insulin resistance independent of nonabdominal and abdominal subcutaneous AT and cardiovascular fitness. Subdivision of visceral and abdominal subcutaneous AT by MRI did not provide additional insight into the relationship between abdominal obesity and metabolic risk in obese men.

Direct effects of gram-negative endotoxin on skeletal muscle glucose uptake

The effect of locally infused endotoxin on gracilis muscle glucose uptake was determined in anesthetized mongrel dogs. Locally infused endotoxin consistently caused an increase in skeletal muscle glucose uptake with no alterations in any other metabolic variable. These data demonstrate that endotoxin can act locally to increase glucose uptake by skeletal muscle, independent of the action of insulin or other metabolic factors. On the other hand, when endotoxin was given systemically to induce shock, gracilis muscle glucose uptake did not increase. These differences may reflect the reduction in plasma endotoxin concentration mediated by the reticuloendothelial system (RES). However, live Escherichia coli shock was associated with an increase in glucose uptake in the constant flow perfused gracilis muscle after 4.5 h of shock. We believe this increase in muscle glucose uptake resulted from the direct effects of endotoxin, the plasma concentration of which presumably increased as the RES was overwhelmed and became less effective. The contribution of this phenomenon to the hypoglycemia of gram-negative endotoxin or septic shock cannot be evaluated from this study.