The adipose tissue metabolism is dependent on its blood perfusion. During lipid mobilization e.g. during exercise and during lipid deposition e.g. postprandial, adipose tissue blood flow is increased. This increase in blood flow may involve capillary recruitment in the tissue. We investigated the basic and postprandial microvascular volume in adipose tissue using real-time contrast-enhanced ultrasound (CEU) imaging in healthy normal weight subjects. In nine subjects, CEU was performed in abdominal subcutaneous adipose tissue and in the underlying skeletal muscle after a bolus injection of ultrasound contrast agent to establish the reproducibility of the technique. In nine subjects, the effect of an oral glucose load on blood flow and microvascular volume was measured in abdominal subcutaneous adipose tissue and forearm skeletal muscle. ¹³³Xe washout and venous occlusion strain-gauge plethysmography was used to measure the adipose tissue and forearm blood flow, respectively. Ultrasound signal intensity of the first plateau phases was 27 ± dB in the abdominal subcutaneous adipose tissue and 18 ± 2 dB (P < 0.05) in the underlying skeletal muscle. The reproducibility of the measurements was good with a 4% coefficient of variation in both tissues. Blood flow and the change in signal intensity as a measure of the microvascular volume increased significantly and simultaneously in abdominal subcutaneous adipose tissue after glucose intake. The forearm blood flow and muscle signal intensity remained constant. It is concluded that the microvascular volume and changes in volume in abdominal subcutaneous adipose tissue can be assessed using CEU with good reproducibility. Postprandial capillary recruitment takes place in abdominal subcutaneous adipose tissue.
In people with type 1 diabetes mellitis (DM), insulin administration, food intake, and exercise have to be carefully matched to avoid either hypo- or hyperglycemia. People with type 2 DM have some insulin secretion, which changes with needs. Accordingly, during exercise, these people do not run the same metabolic risks as people with type 1 DM. However, a contraction-mediated increase in glucose clearance in muscle is intact in type 2 DM. Therefore, in the postabsorptive state in diet-treated type 2 DM, a marked reduction in hyperglycemia can occur during prolonged moderate exercise. Sulfonylurea drugs augment the rate of decline in plasma glucose, because stimulation of insulin secretion reduces hepatic glucose production. After abstention from sulfonylurea for 5 days, the rate of decrease in plasma glucose with exercise is also enhanced, but from a higher glucose level. In the postabsorptive state, brief vigourous exercise elicits an increase in plasma glucose concentration, reflecting an exaggerated counterregulatory hormone response and glucose production. Moreover, insulin sensitivity is reduced in the early postexercise period. In the postprandial state, both prolonged moderate exercise and intermittent high-intensity exercise markedly decrease meal-induced increases in glucose, insulin, and C-peptide concentrations, whereas glucose appearance in plasma is unchanged. When exercise bouts are isocaloric, responses are identical, indicating that overall energy expenditure, and not peak exercise intensity, is the major determinant of exercise-induced changes in overall glucose homeostasis and insulin secretion in type 2 DM. Neither prolonged moderate nor intermittent high-intensity exercise performed in the postprandial state influences glucose or insulin responses to a subsequent meal. Finally, in people with type 2 DM, after a high-fat meal, prolonged moderate exercise reduces the exaggerated increases in plasma concentrations of triglycerides contained in chylomicrons and very low-density lipoproteins.
To elucidate if postprandial exercise can reduce the exaggerated lipidemia seen in type 2 diabetic patients after a high-fat meal. Two mornings eight type 2 diabetic patients (males) (58 +/- 1.2 years, BMI 28.0 +/- 0.9 kg m(-2)) and seven non-diabetic controls ate a high-fat breakfast (680 kcal m(-2), 84% fat). On one morning, 90 min later subjects cycled 60 min at 57% VO(2max). Biopsies from quadriceps muscle and abdominal subcutaneous adipose tissue were sampled after exercise or equivalent period of rest and arterialized blood for 615 min. Postprandial increases in serum total-triglyceride (TG) (incremental AUC: 1,702 +/- 576 vs. 341 +/- 117 mmol l(-1) 600 min), chylomicron-TG (incremental AUC: 1,331 +/- 495 vs. 184 +/- 55 mmol l(-1) 600 min) and VLDL-TG as well as in insulin (incremental AUC: 33,946 +/- 7,414 vs. 13,670 +/- 3,250 pmol l(-1) 600 min), C-peptide and glucose were higher in diabetic patients than in non-diabetic controls (P < 0.05). In diabetic patients these variables were reduced (P < 0.05) by exercise (total-TG incremental AUC being 1,110 +/- 444, chylomicron-TG incremental AUC 1,043 +/- 474 mmol l(-1) 600 min and insulin incremental AUC 18,668 +/- 4,412 pmol l(-1) 600 min). Lipoprotein lipase activity in muscle (11.0 +/- 2.0 vs. 24.1 +/- 3.4 mU g per wet weight, P < 0.05) and post-heparin plasma at 615 min were lower in diabetic patients than in non-diabetic controls, but did not differ in adipose tissue and did not change with exercise. In diabetic patients, 210 min after exercise oxygen uptake (P < 0.05) and fat oxidation (P < 0.1) were still higher than on non-exercise days. In type 2 diabetic patients, after a high-fat meal exercise reduces the plasma concentrations of triglyceride contained in both chylomicrons and VLDL as well as insulin secretion. This suggests protection against progression of atherosclerosis and diabetes.
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