Lipid, Glycemic, and Insulin Responses to Meals Rich in Saturated, cis-Monounsaturated, and Polyunsaturated (n-3 and n-6) Fatty Acids in Subjects With Type 2 Diabetes

Division of Nutrition and Metabolic Diseases, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390, USA.
Diabetes care (Impact Factor: 8.42). 12/2007; 30(12):2993-8. DOI: 10.2337/dc07-1026
Source: PubMed


The recommendations for dietary fats in patients with type 2 diabetes are based largely on the impact of fatty acids on fasting serum lipid and glucose concentrations. How fatty acids affect postprandial insulin, glucose, and triglyceride concentrations, however, remains unclear. The objective of this study was to study the effect of fatty acids on postprandial insulin, glucose, and triglyceride responses.
Test meals rich in palmitic acid, linoleic acid, oleic acid, and eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and containing 1,000 kcal each were administered in a randomized crossover design to 11 type 2 diabetic subjects. Serum insulin, glucose, and triglyceride concentrations were measured for 360 min. All subjects received an isoenergetic diet of constant composition throughout the study.
According to repeated-measures ANOVA, the insulin (P = 0.0002) but not glucose (P = 0.10) response was significantly different between meals. The insulin response was lower to meals rich in oleic acid or EPA and DHA than to meals rich in palmitic acid or linoleic acid (P < 0.01). The triglyceride response did not reach statistical significance (P = 0.06) but tended to be lower with EPA and DHA than with the other fatty acids. Similar trends were seen for area under the curve (AUC) and incremental AUC for serum insulin and triglycerides, but the differences were not significant.
In comparison with palmitic acid and linoleic acid, oleic acid or EPA and DHA may modestly lower insulin response in patients with type 2 diabetes without deteriorating the glucose response. EPA and DHA may also reduce the triglyceride response.

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    • "Several investigations have been developed to evaluate the effect of fatty acid supplementation in the evolution of Type 2 diabetes mellitus [70, 71, 73–81]. Beneficial effects have been described on triacylglycerols, lipoproteins, haemostasia, atherogenic plaque stability, blood pressure, leukocyte function, glucose metabolism, insulin resistance, and even diabetic neuropathy; however, the results depend on dose and duration of intervention. "
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    ABSTRACT: Chronic diseases have become one of the most important public health problems, due to their high costs for treatment and prevention. Until now, researchers have considered that the etiology of Type 2 diabetes mellitus (T2DM) is multifactorial. Recently, the study of the innate immune system has offered an explanation model of the pathogenesis of T2DM. On the other hand, there is evidence about the beneficial effect of polyunsaturated fatty acids (PUFA) n-3 and n-6 in patients with chronic inflammatory diseases including diabetes. Furthermore, high vitamin D plasmatic concentrations have been associated with the best performance of pancreatic β cells and the improving of this disease. In conclusion, certain fatty acids in the adequate proportion as well as 25-hydroxivitamin D can modulate the inflammatory response in diabetic people, modifying the evolution of this disease.
    Journal of Immunology Research 02/2014; 2014(3):860703. DOI:10.1155/2014/860703 · 2.93 Impact Factor
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    • "There are three categories of fatty acids: saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs). Studies have revealed important differences with postprandial lipid responses being of the order SFAs>MUFAs>PUFAs [6-8]. The n-3 and n-6 series PUFAs compete with each other for enzymes required when they are synthesized and all play an important role in vivo [9,10]. "
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    ABSTRACT: Atherosclerosis is a postprandial phenomenon. The balanced n-6/n-3 PUFA ratio contributing to the prevention of atherosclerosis has been well shown, but the effect of the ratio on postprandial metabolism has not been fully investigated. The aim of this study was to investigate the effects of the n-6/n-3 PUFAs ratio on postprandial metabolism in hypertriacylglycerolemia patients, comparing them to healthy controls. Test meals with 0.97 (high n-3) and 8.80 (low n-3) n-6/n-3 PUFAs ratio were administered in a randomized crossover design to 8 healthy and 8 hypertriacylglycerolemia subjects. Blood samples were collected for 8 hours after meals to measure triglyceride (TG), total cholesterol (TC), HDL, ApoA, ApoB, glucose, insulin, inflammatory makers including tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6), endothelial function including nitric oxide (NO) and endothelin-1 (ET-1). According to repeated-measures ANOVA, the postprandial response of lipid, glucose, insulin, inflammation and endothelial function were not significantly different between meals. The postprandial TG and NO response were significantly different between healthy control (HC) and hypertriglyceridemia group (HTG) after both meals (P < 0.01). After both meals maximal change and iAUC for TG was all higher in HTG group than HC group, the difference was significant after low n-3 meal but not after high n-3 meal. The concentration of glucose, insulin, IL-6, TNFalphaand ET-1 at each time point was higher and NO was lower in HTG group, but the maximal change and iAUC had no significant difference except for iAUC of insulin, IL-6 and diAUC of NO after low n-3 meal. The ratio of n-6 and n-3 maybe do not acutely influence the postprandial metabolism, inflammatory response and endothelial function, but the low n-3 meal can strengthen the difference between HTG and HC group.
    Lipids in Health and Disease 12/2013; 12(1):181. DOI:10.1186/1476-511X-12-181 · 2.22 Impact Factor
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    • "Omega-3 disrupts the fatty constructive genes and reduces hormones associated with obesity such as leptin and also prevents the construction of Omega-6 compounds.14 The study of Shah et al has indicated that consumption of Omega-3 improves the effect of insulin in type II diabetic patients without reducing the blood glucose and triglyceride level.15 Friedberg et al revealed that Omega-3 does not affect HbA1c in patients with diabetes and stated that consumption of Omega-3 can reduce 30% of triglyceride level which is appropriate in the treatment of lipid disorders in these patients.16 "
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    ABSTRACT: Visfatin is an adipocytokine which is secreted from adipose tissue and can affect on the diabetes inflammatory reaction and also serum lipids level. On the other hand, Omega-3 can also prevent formation of insulin resistance. In the present study, the effect of Omega-3 on the serum visfatin concentration was evaluated. 71 women with type II diabetes were randomly assigned to the group that took Omega-3 capsules or control group with placebo capsules. In the first step, study subjects filled a questionnaire collecting their age, height, weight, waist circumference, and hip circumference. Also their blood samples were taken for blood tests. In the second step, the intervention was done for 8 weeks and in the third step the aforementioned were collected again. In the blood samples visfatin and lipid profiles (low density lipoprotein [LDL], high density lipoprotein [HDL], triglyceride [TG], and cholesterol), glucose and HbA1c were measured. There was no significant difference in serum visfatin level between Omega-3 and placebo groups before the intervention (p = 0.14), while after the intervention, the mean serum visfatin level in the Omega-3 group was significantly higher (p < 0.001). In addition, the mean difference between the serum visfatin level before and after the intervention in both groups was significant (p < 0.001). This study showed an increase in visfatin level following consuming Omega-3 fats but according to controversial issues on insulin-like function of visfatin, the effects of Omega-3 on diabetes should be studied more in further studies.
    Journal of research in medical sciences 04/2011; 16(4):490-5. · 0.65 Impact Factor
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