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Impact of Fat, Protein, and Glycemic Index on Postprandial Glucose

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Impact of Fat, Protein, and Glycemic Index on Postprandial Glucose 1008 Diabetes Care Volume 38, June 2015 Kirstine J. Bell,1,2 Carmel E. Smart,3,4 Impact of Fat, Protein, and Garry M. Steil,5,6 Jennie C. Brand-Miller,1 Bruce King,3,4 and Howard A. Wolpert2,6 TYPE 1 DIABETES AT A CROSSROADS Glycemic Index on Postprandial Glucose Control in Type 1 Diabetes: Implications for Intensive Diabetes Management in the Continuous Glucose Monitoring Era Diabetes Care 2015;38:1008–1015 | DOI: 10.2337/dc15-0100 BACKGROUND Continuous glucose monitoring highlights the complexity of postprandial glucose patterns present in type 1 diabetes and points to the limitations of current approaches to mealtime insulin dosing based primarily on carbohydrate counting. METHODS A systematic review of all relevant biomedical databases, including MEDLINE, 1Charles Perkins Centre and the School of Molecular Embase, CINAHL, and the Cochrane Central Register of Controlled Trials, was Bioscience, The University of Sydney, Sydney, conducted to identify research on the effects of dietary fat, protein, and glycemic Australia 2Joslin Diabetes Center, Boston, MA index (GI) on acute postprandial glucose control in type 1 diabetes and prandial 3Department of Paediatric Endocrinology and insulin dosing strategies for these dietary factors. Diabetes, John Hunter Children’s Hospital, Newcastle, Australia RESULTS 4Hunter Medical Research Institute, School of All studies examining the effect of fat (n = 7), protein (n =7),andGI(n =7)indicated Medicine and Public Health, University of Newcastle, Rankin Park, Australia that these dietary factors modify postprandial glycemia. Late postprandial hyper- 5Children’s Hospital, Boston, MA glycemia was the predominant effect of dietary fat; however, in some studies, 6Harvard Medical School, Boston, MA glucose concentrations were reduced in the first 2–3 h, possibly due to delayed Corresponding author: Howard A. Wolpert, gastric emptying. Ten studies examining insulin bolus dose and delivery patterns [email protected]. required for high-fat and/or high-protein meals were identified. Because of meth- Received 15 January 2015 and accepted 26 odological differences and limitations in experimental design, study findings were February 2015. inconsistent regarding optimal bolus delivery pattern; however, the studies in- This article contains Supplementary Data online at http://care.diabetesjournals.org/lookup/ dicated that high-fat/protein meals require more insulin than lower-fat/protein suppl/doi:10.2337/dc15-0100/-/DC1. meals with identical carbohydrate content. © 2015 by the American Diabetes Association. Readers may use this article as long as the work CONCLUSIONS is properly cited, the use is educational and not These studies have important implications for clinical practice and patient edu- for profit, and the work is not altered. cation and point to the need for research focused on the development of new See accompanying articles, pp. 968, insulin dosing algorithms based on meal composition rather than on carbohydrate 971, 979, 989, 997, 1016, 1030, and content alone. 1036. care.diabetesjournals.org Bell and Associates 1009 Currently, carbohydrates are consid- the standard of care in the management QUESTION 1: WHAT EFFECTS DO ered the predominant macronutrient of type 1 diabetes (3), the challenges of GI, PROTEIN, AND FAT HAVE ON affecting postprandial glucose control keeping postprandial glucose concentra- ACUTE POSTPRANDIAL GLUCOSE and the primary determinant for calcu- tions in range will become an inescapable CONCENTRATIONS IN TYPE 1 lating mealtime insulin doses in type 1 and increasing focus in the daily lives of DIABETES? diabetes (1). Emerging evidence from people with diabetes. As summarized in Table 1, 16 studies recent research and the use of continu- examining the effects of nutritional fac- ous glucose monitoring have shown SYSTEMATIC REVIEW PROCEDURE tors on postprandial glycemia were that other nutritional properties of For questions 1 and 2, a search of all identified (4–19) (see Supplementary food, including fat, protein, and glyce- relevant biomedical databases was con- Table 1 for more details). mic index (GI), can significantly affect ducted, including MEDLINE, Embase, postprandial glucose excursions. These CINAHL (Cumulative Index to Nursing and Fat findings highlight the need for alterna- Allied Health Literature), Thomson Reu- Seven studies examining the effect of tive mealtime insulin dosing algorithms ters Web of Science (formerly ISI Web of dietary fat on postprandial glycemia in and have important implications for nu- Knowledge), and the Cochrane Central 103 subjects with type 1 diabetes were trition education and counseling in pa- Register of Controlled Trials. The follow- identified (5,7,8,11,15,18,19). All stud- tients with diabetes. ing key words were used to identify ies added fat to the test meal, which The American Diabetes Association potentially relevant articles: “type 1 concurrently increased the energy con- (ADA) recommends that people with di- diabetes” AND “blood glucose” OR “in- tent of the test meal. The amount of di- abetes who have mastered carbohy- sulin” AND “dietary carbohydrate” OR etary fat added to the control meals drate counting receive education on “dietary protein” OR “dietary fat” OR ranged from 6.6 to 52 g. the glycemic impacts of protein and “glycemic index.” The search strategy All studies reported that dietary fat fat (1). To our knowledge, neither a was deliberately broad to identify all rel- modified postprandial glycemia. One comprehensive review of the literature evant articles to answer the two review study did not find an increase in glucose examining the relative effects of pro- questions. concentration (5) possibly because the tein, fat, and GI on postprandial glyce- Original controlled studies were in- postprandial monitoring period was mia nor guidelines for clinicians on how cluded if they were published in English only 3 h. Two studies reported that the insulindosesshouldbeadjustedintype between March 1995 and November addition of dietary fat reduced the area 1 diabetes for various meal composi- 2014, conducted in adults and/or chil- under the curve in the first 2–3 h (7,8). tions exist. dren with type 1 diabetes, used rapid- This may be due to fat delaying gastric This article reviews the evidence ad- acting insulin analogs (lispro, aspart, emptying, as indicated by one of the dressing the following questions: or glulisine), and 1) compared post- studies demonstrating that the gastric prandial glycemia following different emptying rate was significantly reduced 1. What effects do GI, protein, and fat foods/meals with the same insulin dos- in the first 2 h after consuming a high-fat have on acute postprandial glucose ing strategy or 2) different prandial dos- meal (7). This in turn delayed the rise in concentrations in type 1 diabetes? ing strategies for the same foods/meals. postprandial glycemia, with four studies 2. What prandial insulin dosing strate- A start date of March 1995 was inten- reporting a lag in time to peak blood gies work best for GI, protein, and fat tionally chosen because this was when glucose concentrations between 6 and in type 1 diabetes? the first rapid-acting insulin analog (lis- 90 min (mean 29 min) (5,7,15,18). pro) was available in the U.S. Studies of Evidence suggests that meals contain- In light of the evidence reviewed in participants of any age, sex, or race ing carbohydrates and that are high in these questions and our clinical insights, were included. Studies where both the dietary fat cause sustained late post- this article also discusses the following meal and the insulin dose were concur- prandial hyperglycemia. One study questions: rently altered or the meal composition showed the addition of 35 g dietary fat was not controlled and studies in preg- significantly increased postprandial glu- 3. What are the implications for clinical nancy or involving exercise were cose concentrations by 2.3 mmol/L at 5 practice? excluded. h (15). Wolpert et al. (19) demonstrated 4. What are the knowledge gaps, and The literature search identified 143 that the addition of 50 g fat caused sig- how can technology be leveraged to studies, and 13 more studies were iden- nificant hyperglycemia over 5 h, even improve postprandial glucose control? tified through hand-searching refer- when additional insulin was adminis- ence lists (Supplementary Fig. 1). Of tered using a closed-loop glucose con- Current clinical approaches to inten- these studies, 127 were excluded pri- trol system. Free fatty acids (FFAs) sive diabetes management tend to be marily due to duplication (n =23)and directly induce insulin resistance, and insulin-centric; however, a focus on di- not meeting the inclusion criteria for one study postulated that the mecha- etary quality and mealtime routine, this review, including 21 in type 2 dia- nism for the delayed hyperglycemic ef- with referral to a registered dietitian betes, 6 comparing various types of in- fect of dietary fat is FFA-induced insulin for medical nutrition therapy, may be sulin or regimens, and 4 varying insulin resistance with increased hepatic glu- just as important for optimizing glyce- dosing and meals concurrently. The re- cose output (20). Consistent with the mic control (1,2). In the coming years, as maining 29 studies were included in this observed time course of hyperglycemia continuous glucose monitoring becomes review. following higher-fat meals in type 1 1010 Postprandial Glycemia and Insulin Dosing in T1D Diabetes Care Volume 38, June 2015 Table 1—Summary of systematic review: effects of fat, protein, and GI on acute postprandial glycemia in type 1 diabetes Nutritional factor Summary of findings Clinical implications Fat c Seven studies (total 103 subjects) (5,7,8,11,15,18,19). c Increase in dose required for coverage of higher-fat c All studies reported significant differences in meals needs to be individualized. glycemia with addition of fat. c Delicate balance in calculation and timing of insulin c Fat reduces early glucose response (first 2–3 h) (7,8) and action: needs more insulin to prevent late postprandial delays peak blood glucose (5,7,15,18) due hyperglycemia; however, if too much insulin upfront, to delayed gastric emptying.
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