Endocrine and metabolic effects of consuming fructose- and glucose-sweetened beverages with meals in obese men and women: influence of insulin resistance on plasma triglyceride responses

Abstract

Context: Compared with glucose-sweetened beverages, consumption of fructose-sweetened beverages with meals elevates postprandial plasma triglycerides and lowers 24-h insulin and leptin profiles in normal-weight women. The effects of fructose, compared with glucose, ingestion on metabolic profiles in obese subjects has not been studied.

Objective: The objective of the study was to compare the effects of fructose- and glucose-sweetened beverages consumed with meals on hormones and metabolic substrates in obese subjects.

Design and setting: The study had a within-subject design conducted in the clinical and translational research center.

Participants: Participants included 17 obese men (n = 9) and women (n = 8), with a body mass index greater than 30 kg/m(2).

Interventions: Subjects were studied under two conditions involving ingestion of mixed nutrient meals with either glucose-sweetened beverages or fructose-sweetened beverages. The beverages provided 30% of total kilocalories. Blood samples were collected over 24 h.

Main outcome measures: Area under the curve (24 h AUC) for glucose, lactate, insulin, leptin, ghrelin, uric acid, triglycerides (TGs), and free fatty acids was measured.

Results: Compared with glucose-sweetened beverages, fructose consumption was associated with lower AUCs for insulin (1052.6 +/- 135.1 vs. 549.2 +/- 79.7 muU/ml per 23 h, P < 0.001) and leptin (151.9 +/- 22.7 vs. 107.0 +/- 15.0 ng/ml per 24 h, P < 0.03) and increased AUC for TG (242.3 +/- 96.8 vs. 704.3 +/- 124.4 mg/dl per 24 h, P < 0.0001). Insulin-resistant subjects exhibited larger 24-h TG profiles (P < 0.03).

Conclusions: In obese subjects, consumption of fructose-sweetened beverages with meals was associated with less insulin secretion, blunted diurnal leptin profiles, and increased postprandial TG concentrations compared with glucose consumption. Increases of TGs were augmented in obese subjects with insulin resistance, suggesting that fructose consumption may exacerbate an already adverse metabolic profile present in many obese subjects.

Figure 1

Effect of glucose-sweetened beverages (solid lines) and fructose-sweetened beverages (dashed lines) on plasma concentrations of fructose (A), glucose (B), lactate (C), and free fatty acid levels (D) in obese men and women consuming beverages with meals (mean ± sem, n = 17). Fructose was undetectable on the day glucose-sweetened beverages were consumed. Plasma glucose levels were significantly lower (F = 9.0, P < 0.00001, time × treatment), and plasma lactate levels were elevated (F = 13.7 P < 0.00001, time × treatment) after fructose compared with glucose consumption. No significant differences were observed in plasma free fatty acid concentrations between treatments.

Figure 2

Effect of glucose-sweetened beverages (solid lines) andfructose-sweetened beverages (dashed lines) on plasma concentrations of insulin (left panel) and the percent change of plasma leptin from baseline (right panel) in obese human subjects (mean ± sem, n = 17). Plasma insulin (F = 2.15, P < 0.003, time × treatment) and leptin levels (F = 2.55, P < 0.00001, time × treatment) were significantly lower after fructose compared with glucose consumption. Baseline leptin values were 20.7 ± 10.69 (HGl) and 20.3 ± 11.0 (HFr).

Figure 3

Effect of glucose-sweetened beverages (solid lines) and fructose-sweetened beverages (dashed lines) on plasma TG concentrations in obese subjects (mean ± sem, n = 17). Plasma TG levels were significantly elevated after fructose compared with glucose consumption. (F = 4.99 P < 0.0001, treatment × time interaction).

Figure 4

TG responses to consumption of glucose-sweetened (left panel) and fructose-sweetened beverages (right panel) with meals in insulin-sensitive (n = 10, dashed line, round symbol) and insulin-resistant obese subjects (n = 7, solid line, square symbol). Plasma TG concentrations were significantly elevated after fructose consumption in both insulin-sensitive and insulin-resistant subjects (F = 5.1, P < 0.0001, treatment × time).