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      Influence of Fat and Carbohydrate Proportions on the Metabolic Profile in Patients With Type 2 Diabetes: A Meta-Analysis

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          Abstract

          OBJECTIVE

          The effects of dietary macronutrient composition on metabolic profiles in patients with type 2 diabetes have been inconsistent. This meta-analysis aimed to elucidate the effect of replacing dietary fat with carbohydrate on glucose and lipid parameters in patients with type 2 diabetes.

          RESEARCH DESIGN AND METHODS

          We searched for randomized trials that investigated the effects of two kinds of prescribed diets (a low-fat, high-carbohydrate [LFHC] diet and a high-fat, low-carbohydrate [HFLC] diet); in these studies, energy and protein intake did not differ significantly between the two dietary groups. Nineteen studies that included 306 patients met our inclusion criteria. Median diet composition of carbohydrate/fat in the LFHC and HFLC diets was 58%/24% and 40%/40%, respectively.

          RESULTS

          Changes in values for A1C, fasting plasma glucose (FPG), and total and LDL cholesterol did not differ significantly between the LFHC and HFLC groups. However, the LFHC diet significantly increased fasting insulin and triglycerides by 8% ( P = 0.02) and 13% ( P < 0.001), respectively, and lowered HDL cholesterol by 6% ( P < 0.001) compared with the HFLC diet. There were positive associations among the magnitude of changes in FPG, fasting insulin, and triglycerides for the diets analyzed. However, stratified analysis indicated that the increase in triglycerides was insignificant when accompanied by energy intake restriction.

          CONCLUSIONS

          Our findings suggested that replacing fat with carbohydrate could deteriorate insulin resistance while the adverse effect on triglycerides from the LFHC diet could be avoided by restricting energy intake to a degree sufficient for the attainment of weight reduction.

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          Most cited references28

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          Banting lecture 1988. Role of insulin resistance in human disease.

          G M Reaven (1988)
          Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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            Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association.

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              Low-glycemic index diets in the management of diabetes: a meta-analysis of randomized controlled trials.

              The use of diets with low glycemic index (GI) in the management of diabetes is controversial, with contrasting recommendations around the world. We performed a meta-analysis of randomized controlled trials to determine whether low-GI diets, compared with conventional or high-GI diets, improved overall glycemic control in individuals with diabetes, as assessed by reduced HbA(1c) or fructosamine levels. Literature searches identified 14 studies, comprising 356 subjects, that met strict inclusion criteria. All were randomized crossover or parallel experimental design of 12 days' to 12 months' duration (mean 10 weeks) with modification of at least two meals per day. Only 10 studies documented differences in postprandial glycemia on the two types of diet. Low-GI diets reduced HbA(1c) by 0.43% points (CI 0.72-0.13) over and above that produced by high-GI diets. Taking both HbA(1c) and fructosamine data together and adjusting for baseline differences, glycated proteins were reduced 7.4% (8.8-6.0) more on the low-GI diet than on the high-GI diet. This result was stable and changed little if the data were unadjusted for baseline levels or excluded studies of short duration. Systematically taking out each study from the meta-analysis did not change the CIs. Choosing low-GI foods in place of conventional or high-GI foods has a small but clinically useful effect on medium-term glycemic control in patients with diabetes. The incremental benefit is similar to that offered by pharmacological agents that also target postprandial hyperglycemia.
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                Author and article information

                Journal
                Diabetes Care
                diacare
                dcare
                Diabetes Care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                May 2009
                : 32
                : 5
                : 959-965
                Affiliations
                [1] 1Department of Lifestyle Medicine and Applied Nutrition, Ochanomizu University, Tokyo, Japan;
                [2] 2Department of Biostatistic, Epidemiology and Preventive Health Sciences, University of Tokyo, Tokyo, Japan;
                [3] 3Endocrinology and Metabolism, University of Tsukuba, Tsukuba, Japan.
                Author notes
                Corresponding author: Hirohito Sone, sone.hirohito@ 123456ocha.ac.jp
                Article
                1716
                10.2337/dc08-1716
                2671123
                19407076
                5bfd02cc-4a72-4bd0-871f-f7186c4311b2
                © 2009 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. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

                History
                : 22 September 2008
                : 4 February 2009
                Categories
                Reviews/Commentaries/ADA Statements
                Meta-Analysis

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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