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      Differences in Maternal Circulating Fatty Acid Composition and Dietary Fat Intake in Women With Gestational Diabetes Mellitus or Mild Gestational Hyperglycemia

      research-article
      , MD 1 , , PHD 1 , , BA 2 , , MS 1 , , PHD 2
      Diabetes Care
      American Diabetes Association

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          Abstract

          OBJECTIVE

          We investigated the relationship between maternal circulating fatty acids (FAs) and dietary FA intake in pregnant women with gestational diabetes mellitus (GDM; n = 49), women with hyperglycemia less severe than GDM (impaired glucose challenge test [GCT] non-GDM; n = 80), and normal control subjects ( n = 98).

          RESEARCH DESIGN AND METHODS

          A case-control design was nested within a prospective cohort of healthy pregnant women. Fasting concentrations of serum total FAs (enzymatic assay) and FA composition (gas chromatography–mass spectrometry) were determined at entry and the third trimester. Dietary fat intake data were obtained from 24-h recalls.

          RESULTS

          There was a graded increase among groups (control subjects, impaired GCT non-GDM, and GDM) during the third trimester for total FAs and individual FAs, including myristic, palmitic, palmitoleic, oleic, linoleic, linolenic, arachidonic, eicosapentaenoic, and docosahexaenoic acids ( P for trend <0.03 to P < 0.001). Similar relationships were observed at entry in total FAs and for four FAs (myristic, palmitic, palmitoleic, and eicosapentaenoic acids). Women with impaired GCT non-GDM with BMI ≥25 kg/m 2 had the highest levels of FAs at entry, whereas women with GDM with BMI ≥25 kg/m 2 had the highest levels during the third trimester, and all grouped FAs were significantly different from lean women with impaired GCT non-GDM or control subjects ( P < 0.05). Dietary intake of polyunsaturated FAs was decreased, but saturated FAs were increased in GDM compared with impaired GCT non-GDM or control subjects ( P < 0.05).

          CONCLUSIONS

          Abnormalities in fat metabolism are present in both GDM and impaired GCT non-GDM women. Reducing pregravid weight and altering diet might prevent the associated elevation of circulating FAs.

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          Most cited references19

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          Dietary fat intake and risk of type 2 diabetes in women.

          The long-term relations between specific types of dietary fat and risk of type 2 diabetes remain unclear. Our objective was to examine the relations between dietary fat intakes and the risk of type 2 diabetes. We prospectively followed 84204 women aged 34-59 y with no diabetes, cardiovascular disease, or cancer in 1980. Detailed dietary information was assessed at baseline and updated in 1984, 1986, and 1990 by using validated questionnaires. Relative risks of type 2 diabetes were obtained from pooled logistic models adjusted for nondietary and dietary covariates. During 14 y of follow-up, 2507 incident cases of type 2 diabetes were documented. Total fat intake, compared with equivalent energy intake from carbohydrates, was not associated with risk of type 2 diabetes; for a 5% increase in total energy from fat, the relative risk (RR) was 0.98 (95% CI: 0.94, 1.02). Intakes of saturated or monounsaturated fatty acids were also not significantly associated with the risk of diabetes. However, for a 5% increase in energy from polyunsaturated fat, the RR was 0.63 (0.53, 0.76; P < 0.0001) and for a 2% increase in energy from trans fatty acids the RR was 1.39 (1.15, 1.67; P = 0.0006). We estimated that replacing 2% of energy from trans fatty acids isoenergetically with polyunsaturated fat would lead to a 40% lower risk (RR: 0.60; 95% CI: 0.48, 0.75). These data suggest that total fat and saturated and monounsaturated fatty acid intakes are not associated with risk of type 2 diabetes in women, but that trans fatty acids increase and polyunsaturated fatty acids reduce risk. Substituting nonhydrogenated polyunsaturated fatty acids for trans fatty acids would likely reduce the risk of type 2 diabetes substantially.
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            Maternal Lipids as Strong Determinants of Fetal Environment and Growth in Pregnancies With Gestational Diabetes Mellitus

            OBJECTIVE—To determine the contribution of maternal glucose and lipids to intrauterine metabolic environment and fetal growth in pregnancies with gestational diabetes mellitus (GDM). RESEARCH DESIGN AND METHODS—In 150 pregnancies, serum triglycerides (TGs), cholesterol, free fatty acids (FFAs), glycerol, insulin, and glucose were determined in maternal serum and cord blood during the 3rd trimester. Maternal glucose values came from oral glucose tolerance testing and glucose profiles. Measurements of fetal abdominal circumference (AC) were performed simultaneously with maternal blood sampling and birth weight, and BMI and neonatal fat mass were obtained following delivery. RESULTS—Maternal TGs and FFAs correlated with fetal AC size (at 28 weeks: triglycerides, P = 0.001; FFAs, P = 0.02), and at delivery they correlated with all neonatal anthropometric measures (FFA: birth weight, P = 0.002; BMI, P = 0.001; fat mass, P = 0.01). After adjustment for confounding variables, maternal FFAs and TGs at delivery remained the only parameters independently related to newborns large for gestational age (LGA) (P = 0.008 and P = 0.04, respectively). Maternal FFA levels were higher in mothers with LGA newborns than in those with appropriate for gestational age (AGA) newborns (362.8 ± 101.7 vs. 252.4 ± 10.1, P = 0.002). Maternal levels of TGs, FFAs, and glycerol at delivery correlated with those in cord blood (P = 0.003, P = 0.004, and P = 0.005, respectively). Fetal triglyceride and cholesterol levels were negatively correlated with newborn birth weight (P = 0.001), BMI (P = 0.004), and fat mass (P = 0.001). TGs were significantly higher in small for gestational age (SGA) newborns compared with AGA or LGA newborns, while insulin-to-glucose ratio and FFAs were the highest in LGA newborns. CONCLUSIONS—In well-controlled GDM pregnancies, maternal lipids are strong predictors for fetal lipids and fetal growth. Infants with abnormal growth seem to be exposed to a distinct intrauterine environment compared with those with appropriate growth.
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              Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and beta-cell dysfunction.

              Plasma free fatty acids (FFA) play important physiological roles in skeletal muscle, heart, liver and pancreas. However, chronically elevated plasma FFA appear to have pathophysiological consequences. Elevated FFA concentrations are linked with the onset of peripheral and hepatic insulin resistance and, while the precise action in the liver remains unclear, a model to explain the role of raised FFA in the development of skeletal muscle insulin resistance has recently been put forward. Over 30 years ago, Randle proposed that FFA compete with glucose as the major energy substrate in cardiac muscle, leading to decreased glucose oxidation when FFA are elevated. Recent data indicate that high plasma FFA also have a significant role in contributing to insulin resistance. Elevated FFA and intracellular lipid appear to inhibit insulin signalling, leading to a reduction in insulin-stimulated muscle glucose transport that may be mediated by a decrease in GLUT-4 translocation. The resulting suppression of muscle glucose transport leads to reduced muscle glycogen synthesis and glycolysis. In the liver, elevated FFA may contribute to hyperglycaemia by antagonizing the effects of insulin on endogenous glucose production. FFA also affect insulin secretion, although the nature of this relationship remains a subject for debate. Finally, evidence is discussed that FFA represent a crucial link between insulin resistance and beta-cell dysfunction and, as such, a reduction in elevated plasma FFA should be an important therapeutic target in obesity and type 2 diabetes.
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                Author and article information

                Journal
                Diabetes Care
                diacare
                dcare
                Diabetes Care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                September 2010
                : 33
                : 9
                : 2049-2054
                Affiliations
                [1] 1Department of Obstetrics and Gynecology, School of Osteopathic Medicine, University of Medicine and Dentistry of New Jersey, Stratford, New Jersey;
                [2] 2Department of Surgery, School of Osteopathic Medicine, University of Medicine and Dentistry of New Jersey, Stratford, New Jersey.
                Author notes
                Corresponding author: Xinhua Chen, chenx1@ 123456umdnj.edu .
                Article
                0693
                10.2337/dc10-0693
                2928361
                20805277
                97bbde60-d5b5-465e-836d-bbc339697c04
                © 2010 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
                : 14 April 2010
                : 20 May 2010
                Categories
                Original Research
                Pathophysiology/Complications

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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