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      Food Order Has a Significant Impact on Postprandial Glucose and Insulin Levels

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          Abstract

          Postprandial hyperglycemia is an important therapeutic target for optimizing glycemic control and for mitigating the proatherogenic vascular environment characteristic of type 2 diabetes. Existing evidence indicates that the quantity and type of carbohydrate consumed influence blood glucose levels and that the total amount of carbohydrate consumed is the primary predictor of glycemic response (1). Previous studies have shown that premeal ingestion of whey protein, as well as altering the macronutrient composition of a meal, reduces postmeal glucose levels (2–4). There are limited data, however, regarding the effect of food order on postprandial glycemia in patients with type 2 diabetes (5). In this pilot study, we sought to examine the effect of food order, using a typical Western meal, incorporating vegetables, protein, and carbohydrate, on postprandial glucose and insulin excursions in overweight/obese adults with type 2 diabetes. A total of 11 subjects (6 female, 5 male) with metformin-treated type 2 diabetes were studied using a within-subject crossover design. The average (mean ± SD) age and BMI were 54 ± 9 years and 32.9 ± 5 kg/m2, respectively. The average duration of diabetes was 4.8 ± 2.4 years and the mean HbA1c was 6.5 ± 0.7%. After a 12-h overnight fast, subjects consumed an isocaloric meal (628 kcal: 55 g protein, 68 g carbohydrate, and 16 g fat) with the same composition on 2 separate days, 1 week apart. During the first visit, the food order was carbohydrate (ciabatta bread and orange juice), followed 15 min later by protein (skinless grilled chicken breast) and vegetables (lettuce and tomato salad with low-fat Italian vinaigrette and steamed broccoli with butter); the food order was reversed a week later. Blood was sampled for glucose and insulin measurements at baseline (just before meal ingestion) and 30, 60, and 120 min after the start of the meal. The mean postmeal glucose levels were decreased by 28.6% (P = 0.001), 36.7% (P = 0.001), and 16.8% (P = 0.03) at 30, 60, and 120 min, respectively, and the incremental area under the curve (iAUC0–120) was 73% lower (2,001 ± 376.9 vs. 7,545 ± 804.4 mg/dL × 120 min, P = 0.001) when vegetables and protein were consumed first, before carbohydrate, compared with the reverse food order (Table 1). Postprandial insulin levels at 60 and 120 min and the iAUC0–120 were also significantly lower when protein and vegetables were consumed first. Table 1 Glucose and insulin levels/iAUC for various time points/intervals during the two visits Time (min) Carbohydrates first Carbohydrates last P c Change (%) Blood glucose (mg/dL) a 0 106.7 ± 5.3 107.3 ± 6.3 0.752 0.5 30 156.8 ± 8.2 112.0 ± 5.8 0.001 −28.6 60 199.4 ± 12.2 125.6 ± 6.9 0.001 −37.0 120 169.2 ± 13.8 140.8 ± 7.7 0.030 −16.8 Serum insulin (µIU/mL) a 0 18.8 ± 2.4 16.3 ± 1.4 0.154 −13.6 30 62.4 ± 8.6 42.9 ± 9.7 0.083 −31.2 60 125.4 ± 20.1 63.2 ± 11.0 0.002 −49.6 120 152.0 ± 31.7 90.9 ± 16.6 0.014 −40.2 Glucose iAUC (mg/dL × min) b 0–30 751.4 ± 71.0 90.0 ± 26.8 0.001 −88.0 0–60 3,396.8 ± 606.9 444.2 ± 103.8 0.001 −86.9 0–120 7,545.0 ± 804.4 2,001.5 ± 376.9 0.001 −73.5 Insulin iAUC (µIU/mL × min) b 0–30 657.5 ± 131.8 399.5 ± 132.6 0.102 −39.2 0–60 2,908.5 ± 432.0 1,510.5 ± 407.4 0.002 −48.1 0–120 10,097.9 ± 1,646.9 5,202.8 ± 1,061.6 0.002 −48.5 Data are means ± SEM, n = 11. a Blood samples were collected immediately before the meal (t = 0 min) and at 30, 60, and 120 min after the start of the meal. b Intervals were measured in minutes from the start of the meal. c P values were calculated using the Wilcoxon matched-pairs signed rank test. In this pilot study, we demonstrated that the temporal sequence of carbohydrate ingestion during a meal has a significant impact on postprandial glucose and insulin excursions. The magnitude of the effect of food order on glucose levels is comparable to that observed with pharmacological agents that preferentially target postprandial glucose. Moreover, the reduced insulin excursions observed in this experimental setting suggest that this meal pattern may improve insulin sensitivity. A limitation of the study is that we analyzed glucose and insulin responses up to 120 min following meal ingestion, as this study was designed to test postprandial glucose levels as practically measured by patients with type 2 diabetes. Further studies with longer follow-up to delineate the full impact, including delayed effects and the mechanisms underlying the glycemic effect of food order, are indicated. In contrast to conventional nutritional counseling in diabetes, which is largely restrictive and focuses on “how much” and “what not to eat,” this pilot study suggests that improvement in glycemia may be achieved by optimal timing of carbohydrate ingestion during a meal.

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          Most cited references4

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          Dietary carbohydrate (amount and type) in the prevention and management of diabetes: a statement by the american diabetes association.

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            Effect of whey on blood glucose and insulin responses to composite breakfast and lunch meals in type 2 diabetic subjects.

            Whey proteins have insulinotropic effects and reduce the postprandial glycemia in healthy subjects. The mechanism is not known, but insulinogenic amino acids and the incretin hormones seem to be involved. The aim was to evaluate whether supplementation of meals with a high glycemic index (GI) with whey proteins may increase insulin secretion and improve blood glucose control in type 2 diabetic subjects. Fourteen diet-treated subjects with type 2 diabetes were served a high-GI breakfast (white bread) and subsequent high-GI lunch (mashed potatoes with meatballs). The breakfast and lunch meals were supplemented with whey on one day; whey was exchanged for lean ham and lactose on another day. Venous blood samples were drawn before and during 4 h after breakfast and 3 h after lunch for the measurement of blood glucose, serum insulin, glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide 1 (GLP-1). The insulin responses were higher after both breakfast (31%) and lunch (57%) when whey was included in the meal than when whey was not included. After lunch, the blood glucose response was significantly reduced [-21%; 120 min area under the curve (AUC)] after whey ingestion. Postprandial GIP responses were higher after whey ingestion, whereas no differences were found in GLP-1 between the reference and test meals. It can be concluded that the addition of whey to meals with rapidly digested and absorbed carbohydrates stimulates insulin release and reduces postprandial blood glucose excursion after a lunch meal consisting of mashed potatoes and meatballs in type 2 diabetic subjects.
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              Incretin, insulinotropic and glucose-lowering effects of whey protein pre-load in type 2 diabetes: a randomised clinical trial.

              Since protein ingestion is known to stimulate the secretion of glucagon-like peptide-1 (GLP-1), we hypothesised that enhancing GLP-1 secretion to harness its insulinotropic/beta cell-stimulating activity with whey protein pre-load may have beneficial glucose-lowering effects in type 2 diabetes.
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                Author and article information

                Journal
                Diabetes Care
                Diabetes Care
                diacare
                dcare
                Diabetes Care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                July 2015
                11 June 2015
                : 38
                : 7
                : e98-e99
                Affiliations
                Comprehensive Weight Control Center, Division of Endocrinology, Diabetes & Metabolism, Weill Cornell Medical College, New York, NY
                Author notes
                Corresponding author: Alpana P. Shukla, aps2004@ 123456med.cornell.edu .
                Article
                0429
                10.2337/dc15-0429
                4876745
                26106234
                95bb7700-b5d5-4664-b0c3-b62e526290de
                © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
                History
                Page count
                Pages: 2
                Categories
                e-Letters: Observations

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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