![]() Interleukin-6 (IL-6) also influences glucose metabolism by alteration of insulin sensitivity ( 7). Certain cytokines, such as tumor necrosis factor-α (TNF-α), impair insulin action in peripheral tissue ( 5) and have a direct role in obesity-linked insulin resistance ( 6). Hyperglycemia has been shown to induce proinflammatory cytokines and chemokine genes in monocyctic cells ( 4). Return of these values to normal levels with insulin therapy demonstrates a robust anti-inflammatory effect of insulin.ĭiabetes is a chronic inflammatory state associated with insulin resistance ( 1– 3). ![]() We conclude that DKA and NKH are associated with elevation of proinflammatory cytokines, ROS, and cardiovascular risk factors in the absence of obvious infection or cardiovascular pathology. Changes in CRP and homocysteine in response to insulin therapy did not reach control levels after resolution of hyperglycemia. ![]() Circulating levels of cytokines, TBA, DCF, PAI-1, FFAs, cortisol, and GH on admission were significantly increased two- to fourfold in patients with hyperglycemic crises compared with control subjects, and they returned to normal levels after insulin treatment and resolution of hyperglycemic crises. Results were compared with lean and obese control subjects. ![]() #STATVIEW 5.0.1 VERSION 2.0 ACTIVATOR#We measured 1) proinflammatory cytokines (tumor necrosis factor-α, interleukin -6, IL1-β, and IL-8), 2) markers of cardiovascular risk (C-reactive protein, homocysteine, and plasminogen activator inhibitor-1 ), 3) products of reactive oxygen species (ROS thiobarbituric acid -reacting material, and dichlorofluorescein ), and 4) cortisol, growth hormone (GH), and free fatty acids (FFAs) on admission (before insulin therapy) and after insulin therapy and resolution of hyperglycemia and/or ketoacidosis. We studied 20 lean and 28 obese patients with DKA, 10 patients with NKH, and 12 lean and 12 obese nondiabetic control subjects. Acute and chronic hyperglycemia are proinflammatory states, but the status of proinflammatory cytokines and markers of oxidative stress and cardiovascular risks is not known in hyperglycemic crises of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH). ![]()
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