The glycaemic index (GI) concept was originally introduced to classify different sources of carbohydrate (CHO)-rich foods, usually having an energy content of . 80 % from CHO, to their effect on post-meal glycaemia. It was assumed to apply to foods that primarily deliver available CHO, causing hyperglycaemia. Low-GI foods were classified as being digested and absorbed slowly and high-GI foods as being rapidly digested and absorbed, resulting in different glycaemic responses. Low-GI foods were found to induce benefits on certain risk factors for CVD and diabetes. Accordingly it has been proposed that GI classification of foods and drinks could be useful to help consumers make 'healthy food choices' within specific food groups. Classification of foods according to their impact on blood glucose responses requires a standardised way of measuring such responses. The present review discusses the most relevant methodological considerations and highlights specific recommendations regarding number of subjects, sex, subject status, inclusion and exclusion criteria, pre-test conditions, CHO test dose, blood sampling procedures, sampling times, test randomisation and calculation of glycaemic response area under the curve. All together, these technical recommendations will help to implement or reinforce measurement of GI in laboratories and help to ensure quality of results. Since there is current international interest in alternative ways of expressing glycaemic responses to foods, some of these methods are discussed.

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Background: Information is lacking on the potential effect of nҀ3 polyunsaturated fatty acids (PUFAs) on the adipose tissue of patients with type 2 diabetes. Objective: We evaluated whether nҀ3 PUFAs have additional effects on adiposity, insulin sensitivity, adipose tissue function (production of adipokines and inflammatory and atherogenic factors), and gene expression in type 2 diabetes. Design: Twenty-seven women with type 2 diabetes without hypertriglyceridemia were randomly allocated in a double-blind parallel design to 2 mo of 3 g/d of either fish oil (1.8 g nҀ3 PUFAs) or placebo (paraffin oil). Results: Although body weight and energy intake measured by use of a food diary were unchanged, total fat mass (P 0.019) and subcutaneous adipocyte diameter (P 0.0018) were lower in the fish oil group than in the placebo group. Insulin sensitivity was not significantly different between the 2 groups (measured by homeostasis model assessment in all patients and by euglycemichyperinsulinemic clamp in a subgroup of 5 patients per group). By contrast, atherogenic risk factors, including plasma triacylglycerol (P 0.03), the ratio of triacylglycerol to HDL cholesterol (atherogenic index, P 0.03), and plasma plasminogen activator inhibitor-1 (P 0.01), were lower in the fish oil group than in the placebo group. In addition, a subset of inflammation-related genes was reduced in subcutaneous adipose tissue after the fish oil, but not the placebo, treatment. Conclusions: A moderate dose of nҀ3 PUFAs for 2 mo reduced adiposity and atherogenic markers without deterioration of insulin sensitivity in subjects with type 2 diabetes. Some adipose tissue inflammation-related genes were also reduced. These beneficial effects could be linked to morphologic and inflammatory changes in adipose tissue. This trial was registered at clinicaltrials.gov as NCT0037.Am J Clin Nutr 2007;86:1670 -9.