The acute effects of inulin and resistant starch on postprandial serum short-chain fatty acids and second-meal glycemic response in lean and overweight humans.

BACKGROUND/OBJECTIVES: Colonic fermentation of dietary fiber to short-chain fatty acids (SCFA) may protect against obesity and diabetes, but excess production of colonic SCFA has been implicated in the promotion of obesity. We aimed to compare the effects of two fermentable fibers on postprandial SCFA and second-meal glycemic response in healthy overweight or obese (OWO) vs lean (LN) participants. SUBJECTS/METHODS: Using a randomized crossover design, 13 OWO and 12 LN overnight fasted participants were studied for 6 h on three separate days after consuming 300 ml water containing 75 g glucose (GLU) as control or with 24 g inulin (IN) or 28 g resistant starch (RS). A standard lunch was served 4 h after the test drink. RESULTS: Within the entire group, compared with control, IN significantly increased serum SCFA (P<0.001) but had no effect on free-fatty acids (FFA) or second-meal glucose and insulin responses. In contrast, RS had no significant effect on SCFA but reduced FFA rebound (P<0.001) and second-meal glucose (P=0.002) and insulin responses (P=0.024). OWO had similar postprandial serum SCFA and glucose concentrations but significantly greater insulin and FFA than LN. However, the effects of IN and RS on SCFA, glucose, insulin and FFA responses were similar in LN and OWO. CONCLUSIONS: RS has favorable second-meal effects, likely related to changes in FFA rather than SCFA concentrations. However, a longer study may be needed to demonstrate an effect of RS on SCFA. We found no evidence that acute increases in SCFA after IN reduce glycemic responses in humans, and we were unable to detect a significant difference in SCFA responses between OWO vs LN subjects.

Acute increases in serum colonic short-chain fatty acids elicited by inulin do not increase GLP-1 or PYY responses but may reduce ghrelin in lean and overweight humans.

BACKGROUND: Colonic fermentation of dietary fibre to short-chain fatty acids (SCFA) influences appetite hormone secretion in animals, but SCFA production is excessive in obese animals. This suggests there may be resistance to the effect of SCFA on appetite hormones in obesity. OBJECTIVES: To determine the effects of inulin (IN) and resistant starch (RS) on postprandial SCFA, and gut hormone (glucagon-like peptide (GLP-1), peptide-tyrosine-tyrosine (PYY) and ghrelin) responses in healthy overweight/obese (OWO) vs lean (LN) humans. SUBJECTS/METHODS: Overnight-fasted participants (13 OWO and 12 LN) consumed 300 ml water containing 75 g glucose (GLU) as control or 75 g GLU plus 24 g IN, or 28.2 g RS using a randomised, single-blind, cross-over design. Blood for appetite hormones and SCFA was collected at intervals over 6 h. A standard lunch was served 4 h after the test drink. RESULTS: Relative to GLU, IN, but not RS, significantly increased SCFA areas under the curve (AUC) from 4-6 h (AUC4-6). Neither IN nor RS affected GLP-1 or PYY-AUC4-6. Although neither IN nor RS reduced ghrelin-AUC4-6 compared with GLU, ghrelin at 6 h after IN was significantly lower than that after GLU (P<0.05). After IN, relative to GLU, the changes in SCFA-AUC4-6 were negatively related to the changes in ghrelin-AUC4-6 (P=0.017). SCFA and hormone responses did not differ significantly between LN and OWO. CONCLUSIONS: Acute increases in colonic SCFA do not affect GLP-1 or PYY responses in LN or OWO subjects, but may reduce ghrelin. The results do not support the hypothesis that SCFA acutely stimulate PYY and GLP-1 secretion; however, a longer adaptation to increased colonic fermentation or a larger sample size may yield different results.

Effect of ethnicity on glycaemic index: a systematic review and meta-analysis.

OBJECTIVES: Low glycaemic index (GI) foods are recommended to improve glycaemic control in diabetes; however, Health Canada considers that GI food labeling would be misleading and unhelpful, in part, because selected studies suggest that GI values are inaccurate due to an effect of ethnicity. Therefore, we conducted a systematic review and meta-analysis to compare the GI of foods when measured in Caucasians versus non-Caucasians. METHODS: We searched MEDLINE, EMBASE and Cochrane databases for relevant articles. GI differences were aggregated using the generic inverse variance method (random effects model) and expressed as mean difference (MD) with 95% confidence intervals (95% CI). Study quality was assessed based on how well studies complied with official international GI methodology. RESULTS: Review of 1288 trials revealed eight eligible studies, including 28 comparisons of GI among 585 non-Caucasians and 971 Caucasians. Overall, there was borderline significant evidence of higher GI in non-Caucasians than Caucasians (MD, 3.3 (95% CI, -0.1, 6.8); P=0.06) with significant heterogeneity (I(2), 46%; P=0.005). The GI of eight types of rice was higher in non-Caucasians than Caucasians (MD, 9.5 (95% CI, 3.7, 23.1); P=0.001), but there was no significant difference for the other 20 foods (MD, 1.0 (95% CI, -2.5, 4.6); P=0.57). MD was significantly greater in the four low-quality studies (nine comparisons) than the four high-quality studies (19 comparisons; 7.8 vs 0.7, P=0.047). CONCLUSIONS: With the possible exception of rice, existing evidence suggests that GI values do not differ when measured in Caucasians versus non-Caucasians. To confirm these findings high-quality studies using a wide range of foods are required.

Glycemic index, glycemic load and glycemic response: An International Scientific Consensus Summit from the International Carbohydrate Quality Consortium (ICQC).

BACKGROUND AND AIMS: The positive and negative health effects of dietary carbohydrates are of interest to both researchers and consumers. METHODS: International experts on carbohydrate research held a scientific summit in Stresa, Italy, in June 2013 to discuss controversies surrounding the utility of the glycemic index (GI), glycemic load (GL) and glycemic response (GR). RESULTS: The outcome was a scientific consensus statement which recognized the importance of postprandial glycemia in overall health, and the GI as a valid and reproducible method of classifying carbohydrate foods for this purpose. There was consensus that diets low in GI and GL were relevant to the prevention and management of diabetes and coronary heart disease, and probably obesity. Moderate to weak associations were observed for selected cancers. The group affirmed that diets low in GI and GL should always be considered in the context of diets otherwise understood as healthy, complementing additional ways of characterizing carbohydrate foods, such as fiber and whole grain content. Diets of low GI and GL were considered particularly important in individuals with insulin resistance. CONCLUSIONS: Given the high prevalence of diabetes and pre-diabetes worldwide and the consistency of the scientific evidence reviewed, the expert panel confirmed an urgent need to communicate information on GI and GL to the general public and health professionals, through channels such as national dietary guidelines, food composition tables and food labels.

Kinetic model of acetate metabolism in healthy and hyperinsulinaemic humans.

BACKGROUND/OBJECTIVES: The short chain fatty acid acetate (AC), may have a role in increasing insulin sensitivity, thus lowering risk for obesity and type 2 diabetes mellitus. It is unclear if AC kinetics is similar in normal (NI) and hyperinsulinaemic (HI) participants. Therefore, we studied AC absorption from the distal colon in participants with normal (<40 pmol/l) and high (≥40 pmol/l) plasma insulin. This work was a part of a series of studies conceived to compute a kinetic model for AC. Kinetic parameters such as estimates of rate of entry into peripheral blood, hepatic uptake and endogenous/exogenous production were compared in the groups. SUBJECTS/METHODS: Overnight fasted NI (n=9) and HI (n=8) participants were given rectal infusions containing sodium AC (90 mmol/l). The solutions were retained for 40 min, then voided for AC measurement. Total amount of AC infused was 27 mmols. RESULTS: AC absorption from the distal colon (279±103 vs 322±91 µmol/min, P=0.76) and hepatic uptake of AC (155±101 vs 146±85 µmol/min, P=0.94) were similar in the groups. Endogenous and exogenous AC production was significantly higher in NI than HI participants. Plasma AC was inversely proportional to plasma insulin concentrations in the entire cohort (y=k/x, where k=1813). CONCLUSIONS: There was low power to detect differences in AC absorption rate and hepatic AC uptake in NI vs HI. The rate of entry of AC into peripheral blood was similar in NI and HI participants. However, hyperinsulinaemia may alter endogenous and exogenous AC metabolism.

Adiposity, gut microbiota and faecal short chain fatty acids are linked in adult humans.

BACKGROUND/OBJECTIVES: High dietary fibre intakes may protect against obesity by influencing colonic fermentation and the colonic microbiota. Though, recent studies suggest that increased colonic fermentation contributes to adiposity. Diet influences the composition of the gut microbiota. Previous research has not evaluated dietary intakes, body mass index (BMI), faecal microbiota and short chain fatty acid (SCFA) in the same cohort. Our objectives were to compare dietary intakes, faecal SCFA concentrations and gut microbial profiles in healthy lean (LN, BMI⩽25) and overweight or obese (OWOB, BMI>25) participants. DESIGN: We collected demographic information, 3-day diet records, physical activity questionnaires and breath and faecal samples from 94 participants of whom 52 were LN and 42 OWOB. RESULTS: Dietary intakes and physical activity levels did not differ significantly between groups. OWOB participants had higher faecal acetate (P=0.05), propionate (P=0.03), butyrate (P=0.05), valerate (P=0.03) and total short chain fatty acid (SCFA; P=0.02) concentrations than LN. No significant differences in Firmicutes to Bacteroides/Prevotella (F:B) ratio was observed between groups. However, in the entire cohort, Bacteroides/Prevotella counts were negatively correlated with faecal total SCFA (r=-0.32, P=0.002) and F:B ratio was positively correlated with faecal total SCFA (r=0.42, P<0.0001). Principal component analysis identified distinct gut microbiota and SCFA-F:B ratio components, which together accounted for 59% of the variation. F:B ratio loaded with the SCFA and not with the microbiota suggesting that SCFA and F:B ratio vary together and may be interrelated. CONCLUSIONS: The results support the hypothesis that colonic fermentation patterns may be altered, leading to different faecal SCFA concentrations in OWOB compared with LN humans. More in-depth studies looking at the metabolic fate of SCFA produced in LN and OWOB participants are needed in order to determine the role of SCFA in obesity.

Evidence for greater production of colonic short-chain fatty acids in overweight than lean humans.

BACKGROUND: Short-chain fatty acids (SCFA) are produced by colonic microbiota from dietary carbohydrates and proteins that reach the colon. It has been suggested that SCFA may promote obesity via increased colonic energy availability. Recent studies suggest obese humans have higher faecal SCFA than lean, but it is unclear whether this difference is due to increased SCFA production or reduced absorption. OBJECTIVES: To compare rectal SCFA absorption, dietary intake and faecal microbial profile in lean (LN) versus overweight and obese (OWO) individuals. DESIGN: Eleven LN and eleven OWO individuals completed a 3-day diet record, provided a fresh faecal sample and had SCFA absorption measured using the rectal dialysis bag method. The procedures were repeated after 2 weeks. RESULTS: Age-adjusted faecal SCFA concentration was significantly higher in OWO than LN individuals (81.3±7.4 vs 64.1±10.4 mmol kg(-1), P=0.023). SCFA absorption (24.4±0.8% vs 24.7±1.2%, respectively, P=0.787) and dietary intakes were similar between the groups, except for a higher fat intake in OWO individuals. However, fat intake did not correlate with SCFAs or bacterial abundance. OWO individuals had higher relative Firmicutes abundance (83.1±4.1 vs 69.5±5.8%, respectively, P=0.008) and a higher Firmicutes:Bacteriodetes ratio (P=0.023) than LN individuals. There was a positive correlation between Firmicutes and faecal SCFA within the whole group (r=0.507, P=0.044), with a stronger correlation after adjusting for available carbohydrate (r=0.615, P=0.005). CONCLUSIONS: The higher faecal SCFA in OWO individuals is not because of differences in SCFA absorption or diet. Our results are consistent with the hypothesis that OWO individuals produce more colonic SCFA than LN individuals because of differences in colonic microbiota. However, further studies are needed to prove this.

Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials.

BACKGROUND/OBJECTIVES: In the absence of consistent clinical evidence, there are concerns that fructose contributes to non-alcoholic fatty liver disease (NAFLD). To determine the effect of fructose on markers of NAFLD, we conducted a systematic review and meta-analysis of controlled feeding trials. SUBJECTS/METHODS: We searched MEDLINE, EMBASE, CINAHL and the Cochrane Library (through 3 September 2013). We included relevant trials that involved a follow-up of ≥ 7 days. Two reviewers independently extracted relevant data. Data were pooled by the generic inverse variance method using random effects models and expressed as standardized mean difference (SMD) for intrahepatocellular lipids (IHCL) and mean difference (MD) for alanine aminotransferase (ALT). Inter-study heterogeneity was assessed (Cochran Q statistic) and quantified (I(2) statistic). RESULTS: Eligibility criteria were met by eight reports containing 13 trials in 260 healthy participants: seven isocaloric trials, in which fructose was exchanged isocalorically for other carbohydrates, and six hypercaloric trials, in which the diet was supplemented with excess energy (+21-35% energy) from high-dose fructose (+104-220 g/day). Although there was no effect of fructose in isocaloric trials, fructose in hypercaloric trials increased both IHCL (SMD=0.45 (95% confidence interval (CI): 0.18, 0.72)) and ALT (MD=4.94 U/l (95% CI: 0.03, 9.85)). LIMITATIONS: Few trials were available for inclusion, most of which were small, short (≤ 4 weeks), and of poor quality. CONCLUSIONS: Isocaloric exchange of fructose for other carbohydrates does not induce NAFLD changes in healthy participants. Fructose providing excess energy at extreme doses, however, does raise IHCL and ALT, an effect that may be more attributable to excess energy than fructose. Larger, longer and higher-quality trials of the effect of fructose on histopathological NAFLD changes are required.

Glycemic index claims on food labels: review of Health Canada's evaluation.

Recently Health Canada (HC) published its opinion that including glycemic index (GI) values on food labels would be misleading and not add value to nutrition labeling and dietary guidelines to help consumers make healthier food choices. Important areas of concern were identified by HC, but the discussion of them is scientifically invalid. HC concluded that GI has poor precision for labeling purposes based on incorrect application of the standard deviation. In fact, GI methodology is precise enough to distinguish, with high probability, low-GI (GI ≤ 55) from high-GI (GI ≥ 70) foods and to pass the Canadian Food Inspection Agency Nutrition Compliance Test procedure. HC rightly concluded that GI does not respond to portion size, whereas glycemic response does, but no valid evidence was provided to support the assertion that a lower-GI food could have a higher glycemic response. HC's focus on glycemic response could promote a low-carbohydrate diet inconsistent with nutrition recommendations. HC correctly concluded that GI is unresponsive to the replacement of available- with unavailable-carbohydrate but this is irrelevant to GI labeling. HC is rightly concerned about promoting unhealthy low-GI foods; however, this could be avoided by prohibiting GI labeling on such foods. Therefore, HC has provided neither a helpful nor scientifically valid evaluation of GI for labeling purposes but has contributed to the wealth of misinformation about GI in the literature. Currently, Canadian consumers only have access to unregulated and misleading information about GI; well-crafted guidelines for GI labeling would provide consumers accurate information about GI and help them make healthier food choices.

Is glycaemic index (GI) a valid measure of carbohydrate quality?

Recent criticisms of the glycaemic index (GI) focus on its validity with assertions that GI methodology is not valid, GI values are inaccurate and imprecise, GI does not predict what foods are healthy and that whole grain and fibre are better markers of carbohydrate quality than GI. None of the critics provide sound reasons for rejecting GI because some of their arguments are based on flagrant errors in understanding and interpretation while others are not supported by current data or are inconsistent with other nutritional recommendations. This paper addresses current criticisms of GI and outlines reasons why GI is valid: (1) GI methodology is accurate and precise enough for practical use; (2) GI is a property of foods; and (3) GI is biologically meaningful and relevant to virtually everyone. Current dietary guidelines recommend increased consumption of whole grains and dietary fibre but do not mention GI. However, this is illogical because the evidence that GI affects health outcomes is at least as good or better than that for whole grains and fibre. GI is a novel concept from a regulatory point of view and a number of problems need to be addressed to successfully translate GI knowledge into practice. The problems are not insurmountable but no progress can be made until bias and misunderstanding about GI can be overcome and there is better agreement about what is the actual state of knowledge on GI so that the real issues can be identified and addressed.

Altering source or amount of dietary carbohydrate has acute and chronic effects on postprandial glucose and triglycerides in type 2 diabetes: Canadian trial of Carbohydrates in Diabetes (CCD).

BACKGROUND AND AIMS: Nutrition recommendations for type 2 diabetes (T2DM) are partly guided by the postprandial responses elicited by diets varying in carbohydrate (CHO). We aimed to explore whether long-term changes in postprandial responses on low-glycemic-index (GI) or low-CHO diets were due to acute or chronic effects in T2DM. METHODS AND RESULTS: Subjects with diet-alone-treated T2DM were randomly assigned to high-CHO/high-GI (H), high-CHO/low-GI (L), or low-CHO/high-monounsaturated-fat (M) diets for 12-months. At week-0 (Baseline) postprandial responses after H-meals (55% CHO, GI = 61) were measured from 0800 h to 1600 h. After 12 mo subjects were randomly assigned to H-meals or study diet meals (L, 57% CHO, GI = 50; M, 44% CHO, GI = 61). This yielded 5 groups: H diet with H-meals (HH, n = 34); L diet with H- (LH, n = 17) or L-meals (LL, n = 16); and M diet with H- (MH, n = 18) or M meals (MM, n = 19). Postprandial glucose fluctuations were lower in LL than all other groups (p < 0.001). Changes in postprandial-triglycerides differed among groups (p < 0.001). After 12 mo in HH and MM both fasting- and postprandial-triglycerides were similar to Baseline while in MH postprandial-triglycerides were significantly higher than at Baseline (p = 0.028). In LH, triglycerides were consistently (0.18-0.34 mmol/L) higher than Baseline throughout the day, while in LL the difference from Baseline varied across the day from 0.04 to 0.36 mmol/L (p < 0.001). CONCLUSION: Low-GI and low-CHO diets have both acute and chronic effects on postprandial glucose and triglycerides in T2DM subjects. Thus, the composition of the acute test-meal and the habitual diet should be considered when interpreting the nutritional implications of different postprandial responses.

Intravenous acetate elicits a greater free fatty acid rebound in normal than hyperinsulinaemic humans.

BACKGROUND/OBJECTIVES: Colonic fermentation of dietary fiber may improve insulin sensitivity by the metabolic effects of short chain fatty acids (SCFA) in reducing free fatty acids (FFA). The main objectives of this study were to compare peripheral uptake of acetate (AC) in participants with normal (<40 pmol/l, NI) and high (≥ 40 pmol/l, HI) plasma insulin, and the ability of AC to reduce FFA in both the groups. SUBJECTS/METHODS: Overnight fasted NI (n=9) and HI (n=9) participants were given an intravenous (IV) infusion of 140 mmol/l sodium acetate at three different rates over 90 min. The total amount of AC infused was 51.85 mmols. RESULTS: AC clearance in NI participants was not significantly different than that in HI participants (2.11 ± 0.23 vs 2.09 ± 0.24 ml/min). FFA fell in both the groups, but rebounded to a greater extent in NI than HI participants (time × group interaction, P=0.001). Significant correlations between insulin resistance (IR) indices (homeostasis model assessment of insulin resistance (HOMA-IR), Matsuda and insulinogenic index) vs FFA rebound during IV AC infusion were also observed. CONCLUSIONS: These findings suggest that AC uptake is similar in both the groups. Participants with lower plasma insulin and lower IR indices had a greater FFA rebound. These results support the hypothesis that increasing AC concentrations in the systemic circulation may reduce lipolysis and plasma FFA concentrations and thus improve insulin sensitivity. More in-depth studies are needed to look at the effects of SCFA on FFA metabolism in insulin-resistant participants.

Utility of non-high-density lipoprotein cholesterol in assessing incident type 2 diabetes risk.

AIMS: Traditional lipid indices have been associated with type 2 diabetes, but limited data are available regarding non-high-density lipoprotein (non-HDL) cholesterol. In view of recent guidelines for the clinical management of dyslipidemia recommending the monitoring of non-HDL cholesterol as a secondary target after achieving the low-density lipoprotein (LDL) cholesterol goal, we aimed to assess the association of non-HDL cholesterol with incident type 2 diabetes and compare its utility as a risk predictor with traditional lipid variables in Aboriginal Canadians. METHODS: Of 606 diabetes-free participants at baseline, 540 (89.1%) returned for 10-year follow-up assessments. Baseline anthropometry, blood pressure, fasting insulin and serum lipids were measured. Fasting and 2-h postload glucose were obtained at baseline and follow-up to determine the incidence of type 2 diabetes. RESULTS: The cumulative incidence of type 2 diabetes was 17.5%. Higher non-HDL cholesterol, total-to-HDL cholesterol ratio, apolipoprotein B, triglyceride and LDL cholesterol and lower HDL cholesterol concentrations were individually associated with incident type 2 diabetes in univariate analyses (all p < 0.05). Non-HDL cholesterol was a superior determinant of incident diabetes compared with LDL cholesterol (comparing C-statistics of univariate models p = 0.01) or HDL cholesterol (p = 0.004). With multivariate adjustment including waist circumference, non-HDL cholesterol remained associated with incident diabetes [odds ratio (OR) 1.42 (95% confidence interval, CI 1.07-1.88)], while LDL cholesterol and HDL cholesterol became non-significant. CONCLUSIONS: Non-HDL cholesterol was associated with incident type 2 diabetes and was superior to LDL cholesterol as a risk predictor in this population. Further studies are required to establish the utility of non-HDL cholesterol in non-Aboriginal populations.

Inulin increases short-term markers for colonic fermentation similarly in healthy and hyperinsulinaemic humans.

BACKGROUND/OBJECTIVES: Colonic fermentation of dietary fibre produces short-chain fatty acids (SCFAs), acetate, propionate and butyrate, which may protect against type 2 diabetes by reducing serum free-fatty acids (FFAs). Since hyperinsulinaemia is associated with insulin resistance and increased diabetes risk, the main objective was to compare markers of colonic fermentation after acute inulin ingestion in subjects with normal (<40 pmol/l, NI) and high (≥40 pmol/l, HI) plasma insulin. SUBJECTS/METHODS: Overnight fasted NI (n=9) and HI (n=9) subjects were studied for 4 h on two separate days after consuming 300 ml drinks containing 75 g glucose (Glucose) or 75 g glucose plus 24 g inulin (Inulin) using a randomized, single-blind, crossover design. RESULTS: Inulin elicited a higher breath hydrogen and methane areas under the curve (AUC), but the increases in SCFA responses were not statistically significant. Mean serum-acetate concentration over the 4-h study period was higher in NI than in HI subjects (44.3 ± 6.9 vs 22.5 ± 3.7 µmol/l, P=0.001). The rate of rebound of FFA was reduced by Inulin, with FFA at 4 h being less after Inulin than Glucose, regardless of insulin status (0.310 ± 0.028 vs 0.432 ± 0.042 mEq/l, P=0.008). CONCLUSIONS: This suggests that inulin increases short-term markers for colonic fermentation, but a longer study period may be necessary to observe differences in SCFA production. The reason for the lower serum acetate in HI is unclear but may be due to reduced absorption, increased clearance or decreased endogenous production. This suggests the need to compare acetate kinetics in normal and hyperinsulinaemic subjects.

Are the glycemic and insulinemic index values of carbohydrate foods similar in healthy control, hyperinsulinemic and type 2 diabetic patients?

BACKGROUND/OBJECTIVES: a criticism of glycemic index (GI) is that it does not indicate the insulin response of foods (insulinemic index, II). However, it is unknown if the GI and II values of foods are equivalent in all subjects, a necessary criterion for clinical utility. We compared GI and II values in non-diabetic subjects with fasting-serum-insulin (FSI) <40 pmol/l (healthy control) or with FSI ≥ 40 pmol/l (hyper[I]) and subjects with type 2 diabetes (T2DM), and to see whether GI and II were related to the serum-glucose concentrations, insulin sensitivity, ß-cell function and hepatic insulin extraction (HIE) of the subjects. SUBJECTS/METHODS: Serum-glucose, -insulin and -C-peptide responses after 50 g available-carbohydrate portions of glucose (tested three times by each subject), sucrose, instant mashed-potato, white-bread, polished-rice and pearled-barley were measured in healthy control (n=9), hyper[I] (n=12) and T2DM (n=10) subjects. RESULTS: Food GI values did not differ significantly among the three subject groups, whereas II values were higher in T2DM (100±7) than healthy controls (78±5) and hyper[I] subjects (70±5) (mean±s.e.m., P=0.05). II was inversely associated with insulin sensitivity (r=-0.66, P<0.0001) and positively related to fasting- and postprandial-glucose (both r=0.68, P<0.0001) and HIE (r=0.62, P=0.0002). In contrast, GI was not related to any of the biomarkers (P>0.05). CONCLUSION: The GI is a valid property of foods because its value is similar in healthy control, hyper [I] and T2DM subjects, and is independent of subjects' metabolic status. However, II may depend upon the glycaemic control, insulin sensitivity and HIE of the subjects.

Sugars and fat have different effects on postprandial glucose responses in normal and type 1 diabetic subjects.

BACKGROUND AND AIMS: We aimed to determine the effects on glycemic responses and potential risk of hypoglycaemia in type 1 diabetic subjects of replacing half the starch in a meal with sugars, and of adding fat to the low-sugar and high-sugar meals. METHODS AND RESULTS: We studied overnight fasted subjects with type 1 diabetes (n = 11) and age-, BMI- and ethnicity-matched controls (n = 11) using a 2 × 2 factorial design. The low-sugar/low-fat meal was 110 g white-bread. In the high-sugar/low-fat meal half the white-bread starch replaced by sugars (jam and orange juice). The high-fat meals consisted of the low-fat meals plus 20 g fat (margarine). The significance of the main effects of sugars and fat and the sugar × fat, group × sugar and group × fat interactions were determined by ANOVA. In control and diabetic subjects, respectively, high-sugar significantly reduced time to peak rise by 13% (P = 0.004) and 32% (P = 0.004; group × sugar: P = 0.01) and increased peak rise by 14% and 10% (ns). Adding fat increased time to peak rise by 17-19% in both groups (P = 0.003), reduced peak rise by 31% in normal (P < 0.001) but increased peak rise in diabetic subjects by 3% (ns) (group × fat: P = 0.022). Blood glucose nadir and occurrence of hypoglycaemia were similar among the 4 meals. CONCLUSIONS: In type 1 diabetes, insulin adjustment to avoid hypoglycemia may be useful for meals in which the proportion of carbohydrate absorbed as glucose is <0.75, however the precise level which increases hypoglycaemic risk requires further research. The results suggest that people with type 1 diabetes should not be advised to add fat to meals to reduce glycemic responses.