-
1.
Fructose intervention for 12 weeks does not impair glycemic control or incretin hormone responses during oral glucose or mixed meal tests in obese men.
Matikainen, N, Söderlund, S, Björnson, E, Bogl, LH, Pietiläinen, KH, Hakkarainen, A, Lundbom, N, Eliasson, B, Räsänen, SM, Rivellese, A, et al
Nutrition, metabolism, and cardiovascular diseases : NMCD. 2017;(6):534-542
Abstract
BACKGROUND AND AIMS Incretin hormones glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP) are affected early on in the pathogenesis of metabolic syndrome and type 2 diabetes. Epidemiologic studies consistently link high fructose consumption to insulin resistance but whether fructose consumption impairs the incretin response remains unknown. METHODS AND RESULTS As many as 66 obese (BMI 26-40 kg/m2) male subjects consumed fructose-sweetened beverages containing 75 g fructose/day for 12 weeks while continuing their usual lifestyle. Glucose, insulin, GLP-1 and GIP were measured during oral glucose tolerance test (OGTT) and triglycerides (TG), GLP-1, GIP and PYY during a mixed meal test before and after fructose intervention. Fructose intervention did not worsen glucose and insulin responses during OGTT, and GLP-1 and GIP responses during OGTT and fat-rich meal were unchanged. Postprandial TG response increased significantly, p = 0.004, and we observed small but significant increases in weight and liver fat content, but not in visceral or subcutaneous fat depots. However, even the subgroups who gained weight or liver fat during fructose intervention did not worsen their glucose, insulin, GLP-1 or PYY responses. A minor increase in GIP response during OGTT occurred in subjects who gained liver fat (p = 0.049). CONCLUSION In obese males with features of metabolic syndrome, 12 weeks fructose intervention 75 g/day did not change glucose, insulin, GLP-1 or GIP responses during OGTT or GLP-1, GIP or PYY responses during a mixed meal. Therefore, fructose intake, even accompanied with mild weight gain, increases in liver fat and worsening of postprandial TG profile, does not impair glucose tolerance or gut incretin response to oral glucose or mixed meal challenge.
-
2.
Glycaemic load versus carbohydrate counting for insulin bolus calculation in patients with type 1 diabetes on insulin pump.
Bozzetto, L, Giorgini, M, Alderisio, A, Costagliola, L, Giacco, A, Riccardi, G, Rivellese, AA, Annuzzi, G
Acta diabetologica. 2015;(5):865-71
Abstract
AIMS: To evaluate feasibility and effectiveness on short-term blood glucose control of using glycaemic load counting (GLC) versus carbohydrate counting (CC) for prandial insulin dosing in patients with type 1 diabetes (T1D). METHODS Nine T1D patients on insulin pump, aged 26-58 years, HbA1c 7.7 ± 0.8 % (61 ± 8.7 mmol/mol), participated in this real-life setting study. By a crossover design, patients were randomised to calculate their pre-meal insulin dose based on the insulin/glycaemic load ratio (GLC period) or the insulin/carbohydrate ratio (CC period) for 1 week, shifting to the alternate method for the next week, when participants duplicated their first week food plan. Over either week, a blind subcutaneous continuous glucose monitoring was performed, and a 7-day food record was filled in. RESULTS Total daily insulin doses (45 ± 10 vs. 44 ± 9 I.U.; M ± SD, p = 0.386) and basal infusion (26 ± 7 vs. 26 ± 8 I.U., p = 0.516) were not different during GLC and CC periods, respectively. However, the range of insulin doses (difference between highest and lowest insulin dose) was wider during GLC, with statistical significance at dinner (8.4 ± 6.2 vs. 6.0 ± 3.9 I.U., p = 0.041). Blood glucose iAUC after lunch was lower, albeit not significantly, during GLC than CC period (0.6 ± 8.6 vs. 3.4 ± 8.2 mmol/l∙3 h, p = 0.059). Postprandial glucose variability, evaluated as the maximal amplitude after meal (highest minus lowest glucose value), was significantly lower during GLC than CC period at lunch (4.22 ± 0.28 vs. 5.47 ± 0.39 mmol/l, p = 0.002) and dinner (3.89 ± 0.33 vs. 4.89 ± 0.33, p = 0.026). CONCLUSIONS Calculating prandial insulin bolus based on glycaemic load counting is feasible in a real-life setting and may improve postprandial glucose control in people with T1D.
-
3.
A whole-grain cereal-based diet lowers postprandial plasma insulin and triglyceride levels in individuals with metabolic syndrome.
Giacco, R, Costabile, G, Della Pepa, G, Anniballi, G, Griffo, E, Mangione, A, Cipriano, P, Viscovo, D, Clemente, G, Landberg, R, et al
Nutrition, metabolism, and cardiovascular diseases : NMCD. 2014;(8):837-44
Abstract
BACKGROUND AND AIM Until recently, very few intervention studies have investigated the effects of whole-grain cereals on postprandial glucose, insulin and lipid metabolism, and the existing studies have provided mixed results. The objective of this study was to evaluate the effects of a 12-week intervention with either a whole-grain-based or a refined cereal-based diet on postprandial glucose, insulin and lipid metabolism in individuals with metabolic syndrome. METHODS AND RESULTS Sixty-one men and women age range 40-65 years, with the metabolic syndrome were recruited to participate in this study using a parallel group design. After a 4-week run-in period, participants were randomly assigned to a 12-week diet based on whole-grain products (whole-grain group) or refined cereal products (control group). Blood samples were taken at the beginning and end of the intervention, both fasting and 3 h after a lunch, to measure biochemical parameters. Generalized linear model (GLM) was used for between-group comparisons. Overall, 26 participants in the control group and 28 in the whole-grain group completed the dietary intervention. Drop-outs (five in the control and two in the whole-grain group) did not affect randomization. After 12 weeks, postprandial insulin and triglyceride responses (evaluated as average change 2 and 3 h after the meal, respectively) decreased by 29% and 43%, respectively, in the whole-grain group compared to the run-in period. Postprandial insulin and triglyceride responses were significantly lower at the end of the intervention in the whole-grain group compared to the control group (p = 0.04 and p = 0.05; respectively) whereas there was no change in postprandial response of glucose and other parameters evaluated. CONCLUSIONS A twelve week whole-grain cereal-based diet, compared to refined cereals, reduced postprandial insulin and triglycerides responses. This finding may have implications for type 2 diabetes risk and cardiovascular disease.
-
4.
Relationship between smoking habits and the features of the metabolic syndrome in a non-diabetic population.
Masulli, M, Riccardi, G, Galasso, R, Vaccaro, O
Nutrition, metabolism, and cardiovascular diseases : NMCD. 2006;(5):364-70
Abstract
INTRODUCTION Cigarette smoking is a risk factor for type 2 diabetes mellitus. The effect of smoking on the pathogenic factors for the development of diabetes is little explored. We evaluate the relation of smoking with the features of the insulin resistance syndrome, insulin resistance, and insulin secretion. METHODS 2412 non-diabetic men, aged 35-65 years, were studied. Smoking habit was investigated by questionnaire. Anthropometry, blood pressure, forced expiratory volume (FEV1), fasting glucose, triglycerides, total and HDL cholesterol, plasma free fatty acids (FFA), insulin and fibrinogen were measured. HOMA-IR and HOMA beta cell were calculated. The metabolic syndrome was defined according to ATP III criteria. RESULTS The metabolic syndrome was more prevalent in smokers than non-smokers (OR: 1.34; 95% CI 1.01-1.77). This was mainly due to a higher prevalence of dyslipidemia - high triglycerides (46.1% vs 29.9%, p<0.001), or low HDL cholesterol (42.2% vs 30.4%, p<0.001), in smokers. In smokers, other features of insulin resistance - i.e. obesity, hypertension, and hyperglycemia were significantly less frequent and FFA were lower (p<0.001). Plasma insulin and HOMA beta cell were similar in the two groups (8.3 vs 8.0microU/ml and 80.7% vs 82.9%, respectively), but HOMA-IR was significantly lower in smokers (p<0.001) due to the lower glucose values observed in these people. CONCLUSIONS Among the features of the metabolic syndrome, only dyslipidemia is associated with chronic smoking. Smoking in not associated with enhanced insulin resistance, or with impaired insulin secretion. Alternative hypotheses should be explored for the increased risk of diabetes in smokers.
-
5.
Comparative evaluation of simple indices of insulin resistance.
Vaccaro, O, Masulli, M, Cuomo, V, Rivellese, AA, Uusitupa, M, Vessby, B, Hermansen, K, Tapsell, L, Riccardi, G
Metabolism: clinical and experimental. 2004;(12):1522-6
Abstract
Various surrogate methods for the quantification of insulin sensitivity have been proposed. A comparative evaluation is lacking and is relevant for the standardization of investigative methods and comparability of results. The aims of the study were to perform a comparative validation of fasting insulin, homeostasis model assessment (HOMA), Quantitative Insulin Sensitivity Check Index (QUICKI), and revised-QUICKI (R-QUICKI) against minimal model derived estimates of insulin sensitivity (SI(MM)) in nondiabetic people and to carry out a comparative evaluation of the ability of these indices as means for the identification of individuals with the metabolic syndrome (MS) on a population basis. We used 2 data sets defined as "validation sample" and "prevalence sample". Validation sample: a total of 162 healthy men and women aged 30 to 65 years were studied by frequently sampled intravenous glucose tolerance test (FSIVGTT). SI(MM) was calculated with the Minmod program. Prevalence sample: a total of 2,731 nondiabetic men and women aged 35 to 65 years were studied. In both samples, anthropometry, blood pressure, fasting glucose, insulin, triglycerides, high-density lipoprotein (HDL) cholesterol, and free fatty acid (FFA) were measured. HOMA, QUICKI, and R-QUICKI were calculated. The MS was defined according to the Adult Treatment Panel III. Validation sample: insulin, HOMA, QUICKI, and R-QUICKI significantly correlated with SI(MM) (r = -0,53, -0.52, 0.41, 0.33; all P < .001). The finding was confirmed in obese (body mass index [BMI] > or =25 kg/m(2)), but in the normal weight, the correlation coefficient for QUICKI was significantly smaller than for the other indices. Receiver operator characteristic (ROC) curve analysis performed with SI(MM) below or above the lowest 25th percentile (ie, insulin resistance yes, no) as the outcome variable and each of the 4 indices as the test variable showed no significant differences in the areas under the curve. Prevalence sample: prevalence of the MS progressively increased across quartiles of insulin resistance as evaluated by any of the 4 indices, with no significant differences between them. The novel indices QUICKI and R-QUICKI do not perform better than HOMA and fasting insulin as surrogate measures of insulin resistance or means for the identification of people with MS in the general population.
-
6.
Effect of insulin and sulfonylurea therapy, at the same level of blood glucose control, on low density lipoprotein subfractions in type 2 diabetic patients.
Rivellese, AA, Patti, L, Romano, G, Innelli, F, Di Marino, L, Annuzzi, G, Iavicoli, M, Coronel, GA, Riccardi, G
The Journal of clinical endocrinology and metabolism. 2000;(11):4188-92
Abstract
The aim of this study was to evaluate the effect of sc insulin (INS) compared with sulfonylurea (SUL) therapy, at the same level of blood glucose control, on the low density lipoprotein (LDL) subfraction profile in normolipidemic type 2 diabetic patients. Nine normolipidemic type 2 diabetic men (age, 56+/-3 yr; body mass index, 26.5+/-0.9 kg/m2; mean +/- SEM), after a 3-week wash-out period, were assigned to INS or SUL for 2 months in a randomized cross-over design. Doses were adjusted only during the first month and then were kept constant. At the end of the treatments, hemoglobin A1c, plasma lipids, LDL, and very low density lipoprotein (VLDL) subfraction profiles and plasma postheparin lipoprotein lipase and hepatic lipase (HL) activities were evaluated. Despite glucose control was similar at the end of both periods (hemoglobin A1c, 7.4+/-0.3% vs. 7.0+/-0.2%, INS vs. SUL), INS compared with SUL significantly reduced plasma triglyceride (0.9+/-0.1 vs. 1.1+/-0.1 mmol/L; P < 0.05). Although INS did not affect the LDL concentration, it induced a decrease in both the amount (59.0 = 9.8 vs. 76.1+/-16.8 mg/dL; P = NS) and the proportion (31.2+/-3.0% vs. 38.3+/-3.8%; P < 0.03) of small LDL. Moreover, the decrease in small LDL was positively related to the reduction of large VLDL (r = 0.67; P < 0.04) and HL (r = 0.69, P < 0.05) induced by insulin therapy. In conclusion, sc insulin therapy, independently of glucose control and even in the presence of quite low plasma triglyceride levels, is able to reduce small LDL particles in type 2 diabetic patients. This change is related to decreases in both HL activity and large VLDL particles.