Few studies have examined the influence of pre-exercise meals with different glycaemic indices (GIs) on substrate oxidation and non-homeostatic appetite (i.e. food reward) in adults of various ages and ethnicities. We aimed to examine the effects of pre-exercise high and low GI meals on substrate oxidation and food reward in middle-aged Japanese women. This randomised crossover trial included fifteen middle-aged women (aged 40⋅9 ± 6⋅5 years, mean ± sd). The participants consumed a high or low GI breakfast at 09.00 and rested until 11.00. Thereafter, participants performed a 60-min walk at 50 % of their estimated maximum oxygen uptake (11.00–12.00) and rested until 13.00. Expired gas samples were collected every 30 min prior to walking, and samples were collected continuously throughout the walking and post-walking periods. Blood samples and subjective appetite ratings were collected every 30 min, except during walking. The Leeds Food Preference Questionnaire in Japanese (LFPQ-J) was used to assess food reward at 09.00, 10.00, and 13.00 h. The cumulative fat oxidation during exercise was higher in the low GI trial than in the high GI trial (P = 0⋅03). The cumulative carbohydrate oxidation during walking was lower in the low GI trial than in the high GI trial (P = 0⋅01). Trial-by-time interactions were not found for any food-reward parameters between trials. Low GI meals elicited enhanced fat oxidation during a subsequent 60-min walk in middle-aged women. However, meals with different GIs did not affect food reward evaluated over time in the present study.

The effect of modifying dietary fatty acid (FA) composition on insulin sensitivity remains unclear. We aimed to investigate whether changes in plasma phospholipid (PL) FA composition, as a result of dietary intervention, correspond with changes in insulin sensitivity. The RISCK study was a 6-month randomised controlled dietary intervention study, which assessed the effect of modifying dietary fat and the glycaemic index (GI) of carbohydrates on insulin sensitivity. Total NEFA levels, fasting plasma PL FA profiles and an insulin sensitivity index (Si), derived from intravenous glucose tolerance minimal-model analysis, were available from 533 participants, all at elevated risk of type 2 diabetes. Bivariate correlations between changes in saturated PL FA (SFA), MUFA (as a percentage of total plasma NEFA) and changes in Si were assessed according to treatment group. Age, sex, ethnicity, percentage change in body mass and change in dietary GI were controlled for. Increasing total NEFA concentration was associated with worsening Si (r −0·152; P = 0·001). In the high-MUFA/low-GI diet group, change in PL-MUFA was positively and independently associated with change in Si (r 0·297; P = 0·002). Among MUFA, change in oleic acid (18 : 1) was most strongly correlated with change in Si (r 0·266; P = 0·005), as was change in minor FA 24 : 1 (r 0·244; P = 0·011) and 17 : 1 (r 0·196; P = 0·042). In the high-SFA/high-GI group, change in SFA concentration was not significantly associated with change in Si. In conclusion, increases in the proportion of plasma PL-MUFA following a high-MUFA dietary intervention were associated with improvements in insulin sensitivity.

Elevated postprandial glycaemia has been linked to CVD in a number of different epidemiological studies involving predominantly non-diabetic volunteers. The MiniMed continuous glucose monitor, which measures blood glucose every 5 min, over a 24 h period, was used to investigate changes in blood glucose readings before and after instigating a diet with low glycaemic index (GI) for 1 week in free-living healthy individuals. Nine healthy people (age 27 (sem 1·3) years, BMI 23·7 (sem 0·7) kg/m2, one male, eight females) completed the study. A reduction in GI (59·7 (sem 2) v. 52·1 (sem 2), P<0·01) occurred in all nine subjects while energy and other macronutrients remained constant. A significant reduction was also observed in fasting glucose at 06·00 hours (5·4 (sem 0·2) v. 4·4 (sem 0·3) mmol/l, P<0·001), mean glucose (5·6 (sem 0·2) v. 5·1 (sem 0·2) mmol/l, P=0·004), area under the 24 h glucose curve (8102 (sem 243) v. 750 (sem 235) mmol/l per min, P=0·004) and area under the overnight, 8 h glucose curve (2677 (sem 92) v. 2223 (sem 121) mmol/l per min, P=0·01). The present study provides important data on how a simple adjustment to the diet can improve glucose profiles that, if sustained in the long term, would be predicted from epidemiological studies to have a favourable influence on CVD.

Several epidemiological studies link consumption of fibre-rich foods to a reduced risk of type 2 diabetes and CHD. The ‘fibre hypothesis’ suggested that this was a direct effect of fibre. However, fibre-rich foods contain different types of fibre as well as other potentially beneficial compounds, and many foods naturally high in fibre have low glycaemic and insulinaemic indices, possibly due to food form. The question therefore emerges as to the effect of isolated fibre per se on insulin sensitivity, lipids and other risk factors associated with the metabolic syndrome. Many beneficial effects are seen with pharmacological doses of isolated viscous soluble fibre, including improved insulin sensitivity, decreased LDL-cholesterol levels and decreased clotting factors. Similar effects are seen with low glycaemic-index foods. In contrast, insoluble non-viscous cereal fibre is not seen to act directly on risk factors when taken in refined foods such as in milled flour. Since cereal fibre, the major type of fibre in western diets, does not directly act on the risk factors for the metabolic syndrome, the question remains as to possible mechanisms. Until now, fibre and the nature and processing of the starch and particle size have been seen as the main determinants of the metabolic response to starchy foods. However, fibre-rich foods also have an increased protein-to-carbohydrate ratio. Hence we suggest that the protective effect of fibre may also be due to increased vegetable protein content, which may act directly to reduce clotting factors and oxidized LDL-cholesterol levels.