Objectives: We examined the effects of a combined 7-d low–glycemic index (low-GI) diet and exercise training intervention on insulin sensitivity in older obese humans.

Design: Participants [n = 32; mean (±SEM) age: 66 ± 1 y; body mass index (in kg/m²): 33.8 ± 0.7] were randomly assigned to a parallel, double-blind, controlled-feeding trial and underwent supervised aerobic exercise (EX; 60 min/d at 80–85% maximum heart rate) in combination with either a low-GI (LoGI + EX: 41.1 ± 0.4) or a high-GI (HiGI + EX: 80.9 ± 0.6) diet. All meals were provided and were isocaloric to individual energy requirements. Insulin sensitivity and hepatic glucose production were assessed with a 40–mU ⋅ m^–2 · min^–1 hyperinsulinemic euglycemic clamp combined with a [6,6-²H₂]-glucose infusion.

Results: After the intervention, small decreases were observed in body weight (–1.6 ± 0.2 kg; P < 0.0001) and fat mass (–1.7 ± 0.9%; P = 0.004) in both groups. Maximal aerobic capacity ( O₂max) also improved slightly (0.06 ± 0.02 L/min; P = 0.004). Resting systolic blood pressure, fasting glucose, insulin, triglycerides, and cholesterol all decreased after the study (all P < 0.05). Larger changes in systolic blood pressure and O_2max were seen in the LoGI + EX group. Insulin-stimulated glucose disposal (P < 0.001), insulin suppression of hepatic glucose production (P = 0.004), and postabsorptive fat oxidation (P = 0.03) improved equally in both groups after the intervention.

Conclusions: These findings suggest that the metabolic improvements after short-term exercise training in older obese individuals are dependent on increased physical activity and are not influenced by a low-GI diet. However, a low-GI diet has added benefit in alleviating hypertension, thus reducing the risk of diabetic and vascular complications.

Objective: Our aim was to examine cross-sectional and longitudinal associations between circulating forms of osteocalcin (total, uncarboxylated, and carboxylated) and insulin resistance in older men and women.

Design: Cross-sectional associations between serum measures of total osteocalcin, carboxylated osteocalcin, and uncarboxylated osteocalcin and insulin resistance were examined in 348 nondiabetic men and women (mean age: 68 y; 58% female) by using the homeostasis model assessment of insulin resistance (HOMA-IR). Associations between each form of osteocalcin at baseline and 3-y change in HOMA-IR were examined in 162 adults (mean age: 69 y; 63% female) who did not receive vitamin K supplementation.

Results: Lower circulating uncarboxylated osteocalcin was not associated with higher HOMA-IR at baseline or at 3-y follow-up. Those in the lowest tertiles of total osteocalcin and carboxylated osteocalcin at baseline had higher baseline HOMA-IR (P = 0.006 and P = 0.02, respectively). The concentration of carboxylated osteocalcin at baseline was inversely associated with a 3-y change in HOMA-IR (P = 0.002).

Conclusions: In older adults, circulating uncarboxylated osteocalcin was not associated with insulin resistance. In contrast, elevated carboxylated osteocalcin and total osteocalcin were associated with lower insulin resistance, which supports a potential link between skeletal physiology and insulin resistance in humans. The role of vitamin K status in this association remains unclear and merits further investigation. This trial is registered at clinicaltrials.gov as NCT00183001.

Objective: Our aim was to examine the effects of prebiotic supplementation on satiety and related hormones during a test meal for human volunteers by using a noninvasive micromethod for blood sampling to measure plasma gut peptide concentrations.

Design: This study was a randomized, double-blind, parallel, placebo-controlled trial. A total of 10 healthy adults (5 men and 5 women) were randomly assigned to groups that received either 16 g prebiotics/d or 16 g dextrin maltose/d for 2 wk. Meal tolerance tests were performed in the morning to measure the following: hydrogen breath test, satiety, glucose homeostasis, and related hormone response.

Results: We show that the prebiotic treatment increased breath-hydrogen excretion (a marker of gut microbiota fermentation) by 3-fold and lowered hunger rates. Prebiotics increased plasma glucagon-like peptide 1 and peptide YY concentrations, whereas postprandial plasma glucose responses decreased after the standardized meal. The areas under the curve for plasma glucagon-like peptide 1 and breath-hydrogen excretion measured after the meal (0–60 min) were significantly correlated (r = 0.85, P = 0.007). The glucose response was inversely correlated with the breath-hydrogen excretion areas under the curve (0–180 min; r = –0.73, P = 0.02).

Conclusion: Prebiotic supplementation was associated with an increase in plasma gut peptide concentrations (glucagon-like peptide 1 and peptide YY), which may contribute in part to changes in appetite sensation and glucose excursion responses after a meal in healthy subjects.

Objective: We assessed the utility of a food insulin index (FII) that was based on testing isoenergetic portions of single foods (1000 kJ) in predicting the insulin demand evoked by composite meals.

Design: Healthy subjects (n = 10 or 11 for each meal) consumed 13 different isoenergetic (2000 kJ) mixed meals of varying macronutrient content. Insulin demand predicted by the FII of the component foods or by carbohydrate counting and glycemic load was compared with observed insulin responses.

Results: Observed insulin responses (area under the curve relative to white bread: 100) varied over a 3-fold range (from 35 ± 5 to 116 ± 26) and were strongly correlated with insulin demand predicted by the FII of the component foods (r = 0.78, P = 0.0016). The calculated glycemic load (r = 0.68, P = 0.01) but not the carbohydrate content of the meals (r = 0.53, P = 0.064) also predicted insulin demand.

Conclusions: The relative insulin demand evoked by mixed meals is best predicted by a physiologic index based on actual insulin responses to isoenergetic portions of single foods. In the context of composite meals of similar energy value, but varying macronutrient content, carbohydrate counting was of limited value.

Objective: The objective was to assess glycemic control in type 2 diabetic subjects and healthy lean and obese control subjects under strict dietary standardization but otherwise free-living conditions, with and without the consumption of soft drinks.

Design: Obese type 2 diabetic men (n = 11) and lean (n = 10) and obese (n = 10) normoglycemic male control subjects participated in a randomized crossover study. The subjects were provided with a standardized diet in 2 periods, during which they consumed 250 mL water with or without (control) sucrose (37.5 g) 2 h after breakfast and lunch. Blood glucose concentrations were assessed by continuous glucose monitoring.

Results: In the type 2 diabetic subjects, the mean 24-h glucose concentrations were significantly elevated (9.1 ± 0.6 mmol/L), and hyperglycemia (glucose >10 mmol/L) was evident over 33 ± 8% (8 ± 2 h) of a 24-h period (P < 0.01). Hyperglycemia was rarely present in the normoglycemic lean and obese control subjects (5 ± 2%/24 h for both). Consumption of 75 g sucrose, equivalent to 2 cans of a soft drink, did not further augment the prevalence of hyperglycemia throughout the day in any group.

Conclusions: Type 2 diabetic subjects taking oral blood glucose–lowering medication experience hyperglycemia during most of the daytime. Moderate consumption of sucrose-sweetened beverages does not further increase the prevalence of hyperglycemia in type 2 diabetic subjects or in normoglycemic lean or obese men.

Objectives: The objectives were to determine the effect of lysine ingestion on insulin and glucagon concentrations and whether the effect is moderated by glucose ingestion.

Design: Thirteen healthy subjects were studied on 4 occasions. Water, 25 g glucose, 1 mmol lysine/kg lean body mass, or lysine plus glucose was given on separate occasions at 0800 after a 12-h fast. Serum lysine, glucose, insulin, and glucagon were measured during a 2.5-h period. The amount of lysine provided was equivalent to that present in a 672-g (24-oz) steak.

Results: Lysine ingestion resulted in an 3-fold increase in lysine concentration and in a small decrease in glucose concentration. When lysine was ingested with glucose, the 2.5-h glucose area response decreased by 44% (P < 0.02). Lysine alone increased the insulin area response modestly; the insulin increase when lysine was ingested with glucose was similar to that when only glucose was ingested. Lysine stimulated an increase in glucagon (P < 0.02), whereas glucose decreased glucagon.

Conclusions: Lysine ingestion results in a small decrease in serum glucose and an increase in glucagon and insulin concentrations. Lysine ingested with glucose dramatically attenuated the glucose-stimulated glucose response, but there was no change in insulin response. Whether similar effects will be observed with more physiologic doses of lysine remains to be determined.