Substrate utilization in non-obese Type II diabetic patients at rest and during exercise

Abstract

Recently, we observed that impairments exist in skeletal muscle free fatty acid (FFA) utilization during exercise in obese subjects with Type II diabetes. The main objective of the present study was to investigate whether plasma FFA oxidation is impaired during exercise in non-obese Type II diabetic patients. Stable isotope tracers of palmitate and glucose were infused for 2 h at rest and 1h of bicycle exercise at 40% peak oxygen consumption ( V*O(2)max) in volunteers with Type II diabetes and a healthy control group. At rest, plasma FFA oxidation was not significantly different between subjects with Type II diabetes and control subjects (2.13+/-0.51 versus 1.93+/-0.54 micromol.kg(-1).min(-1) respectively). During exercise, Type II diabetic patients and control subjects had similar rates of total fat [Type II diabetes, 9.62+/-1.84 micromol.kg(-1).min(-1); control, 12.08+/-4.59 micromol.kg(-1).min(-1); not significant (NS)] and glucose oxidation (Type II diabetes, 44.24+/-10.36 micromol.kg(-1).min(-1); control, 57.37+/-14.54 micromol.kg(-1).min(-1); NS). No aberrations were present in plasma FFA uptake [rate of disappearance ( Rd ); Type II diabetes, 11.78+/-4.82; control, 10.84+/-3.39; NS] and oxidation rates (Type II diabetes 8.10+/-1.44; control 8.00+/-3.12, NS) in Type II diabetic patients; triacylglycerol-derived fatty acid oxidation was 2.6-fold lower in Type II diabetic patients than in control subjects, but this difference was not statistically significant. Muscle glycogen oxidation was lower in diabetes patients than in control subjects (Type II diabetes, 25.16+/-13.82 micromol.kg(-1).min(-1); control, 42.04+/-10.58 micromol.kg(-1).min(-1); P<0.05) and plasma glucose contributed more to energy expenditure in Type II diabetes (26+/-3% in diabetic versus 15+/-2% in control, P <0.05). We conclude that plasma FFA oxidation is not impaired during exercise in non-obese Type II diabetic patients. The data confirm that Type II diabetes is a heterogeneous disease, and that the adaptation at the substrate level differs between obese and non-obese patients and may contribute to differences in the final appearance of the various phenotypes.

Substrate source utilisation in long-term diagnosed type 2 diabetes patients at rest, and during exercise and subsequent recovery

“…Fasting whole-body fat oxidation rates were greater in the diabetes patients. This seems to be in contrast to some [14][15][16][17][18][19], but not all [12,13,36], previous studies, which describe normal and/or decreased basal whole-body fatty acid oxidation rates in the type 2 diabetic state [14][15][16][17][18][19]. These apparently contradictory findings are explained by the fact that long-term-diagnosed diabetes patients were selected to participate in the present study.…”

“…Pretesting Maximal workload capacity (W max ) and maximal oxygen uptake capacity (VO 2max ) were determined with an electronically braked cycle ergometer (Excalibur, Lode, Groningen, the Netherlands) during an incremental exhaustive exercise test 2 weeks prior to the first trial [17]. Oxygen uptake (VO 2 ) and carbon dioxide production (VCO 2 ) were measured with an Oxycon β (Mijnhart, Breda, the Netherlands).…”

“…In these patients, basal oxidation rates of whole-body total fat have been reported to be both increased [11][12][13] and similar [14][15][16][17][18][19] compared with lean [11][12][13] and overweight/obese [14][15][16][17][18][19] controls respectively. Whole-body plasma NEFA uptake and/or oxidation rates at rest have been reported to be either similar [17,18] or decreased [16] in the type 2 diabetes patient. However, data on arteriovenous differences in plasma NEFA concentrations over the leg or arm have more consistently displayed reduced fasting plasma NEFA uptake and/or oxidation in type 2 diabetes patients compared with normoglycaemic controls [11,14,20], despite elevated systemic plasma NEFA and glucose levels [14,20].…”

“…However, data on arteriovenous differences in plasma NEFA concentrations over the leg or arm have more consistently displayed reduced fasting plasma NEFA uptake and/or oxidation in type 2 diabetes patients compared with normoglycaemic controls [11,14,20], despite elevated systemic plasma NEFA and glucose levels [14,20]. During exercise, in both the prediabetes and/or type 2 diabetes state, the uptake and oxidation of plasma NEFA and other lipid sources have been shown to be similar [17,18] or decreased [16,21]. A cross-sectional review of the literature on the use of lipoprotein and/or muscle-derived triacylglycerol suggests that type 2 diabetes patients have a reduced capacity to mobilise and/or oxidise the intramyocellular lipid stores [22].…”

“…This can be attributed to a blunted increase in hepatic glucose output [23] and/or an increase in whole-body glucose uptake rate [15,17,18,24]. The latter has been shown to result in greater carbohydrate oxidation rates during exercise in type 2 diabetes patients in some [24] but not all studies [15][16][17][18].…”