A human model of dietary saturated fatty acid induced insulin resistance

Koška, Juraj; Ozias, Marlies K.; Deer, James; Kurtz, Julie; Salbe, Arline D.; Harman, S. Mitchell; Reaven, Peter D.

doi:10.1016/j.metabol.2016.07.015

Cited by 59 publications

(43 citation statements)

References 32 publications

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“…In the present study we used our recently described model of feeding a high SFA diet for 24 hours to induce insulin resistance . Three weeks of treatment with liraglutide partially ameliorated the high SFA diet‐induced increase in SSPG 150–180 , indicating improvement in whole‐body insulin sensitivity.…”

Section: Discussionmentioning

confidence: 99%

“…In the present study we used our recently described model of feeding a high SFA diet for 24 hours to induce insulin resistance. 6 Three Skeletal muscle is considered to be the primary site of peripheral insulin resistance. 26,27 Intact microvascular function is critical for timely insulin delivery and glucose utilization in skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

“…On the last day of each treatment arm, overnight‐fasted (>10 hours) participants arrived at the clinical research unit to begin a hypercaloric, high‐fat diet consisting of liquid shakes, with fat supplying ~80% of calories for breakfast, lunch, dinner and a bedtime snack (15% carbohydrates and 5% proteins), as previously described . The amount of fat per meal was 65 g/m 2 of body surface area for breakfast, lunch and dinner meals, and 32.5 g/m 2 for bedtime snack.…”

Section: Methodsmentioning

confidence: 99%

“…Insulin resistance is closely linked to a variety of conditions, including dyslipidaemia, hyperglycaemia, hypertension, inflammation and endothelial dysfunction . It can be rapidly induced by high‐fat Western diets in the absence of significant weight gain . Ingestion of high‐fat meals leads to postprandial rises in triglyceride‐rich lipoproteins and spillover release of fatty acids to adipose tissue, skeletal muscle and liver, interfering with insulin action on glucose metabolism .…”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3] It can be rapidly induced by high-fat Western diets in the absence of significant weight gain. [4][5][6] Ingestion of highfat meals leads to postprandial rises in triglyceride-rich lipoproteins and spillover release of fatty acids to adipose tissue, skeletal muscle and liver, interfering with insulin action on glucose metabolism. 7,8 Fatty acids also impair vasodilatory action of insulin in the microvasculature, diminishing insulin delivery to skeletal muscle.…”

Section: Introductionmentioning

confidence: 99%

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Effect of liraglutide on dietary lipid‐induced insulin resistance in humans

Koska

Lopez

D'Souza

et al. 2017

Diabetes Obesity Metabolism

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Aims: To test whether liraglutide suppresses postprandial elevations in lipids and thus protects against high saturated fatty acid (SFA) diet-induced insulin resistance. Methods:In a randomized placebo-controlled crossover study, 32 participants with normal or mildly impaired glucose tolerance received liraglutide and placebo for 3 weeks each. Insulin suppression tests (IST) were conducted at baseline and after a 24-hour SFA-enriched diet after each treatment. Plasma glucose, insulin, triglycerides and non-esterified fatty acids (NEFA) were measured over the initial 8 hours (breakfast and lunch) on the SFA diet. A subset of participants underwent ex vivo measurements of insulin-mediated vasodilation of adipose tissue arterioles and glucose metabolism regulatory proteins in skeletal muscle.Results: Liraglutide reduced plasma glucose, triglycerides and NEFA concentrations during the SFA diet (by 50%, 25% and 9%, respectively), and the SFA diet increased plasma glucose during the IST (by 36%; all P < .01 vs placebo). The SFA diet-induced impairment of vasodilation on placebo (−9.4% vs baseline; P < .01) was ameliorated by liraglutide (−4.8%; P = .1 vs baseline).In skeletal muscle, liraglutide abolished the SFA-induced increase in thioredoxin-interacting protein (TxNIP) expression (75% decrease; P < .01 vs placebo) and increased 5 0 AMP-activated protein kinase (AMPK) phosphorylation (50% vs −3%; P = .04 vs placebo).Conclusions: Liraglutide blunted the SFA-enriched diet-induced peripheral insulin resistance.This effect may be related to improved microvascular function and modulation of TxNIP and AMPK pathways in skeletal muscle. K E Y W O R D Sinsulin resistance, liraglutide, randomised trial

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Effect of liraglutide on dietary lipid‐induced insulin resistance in humans

Koska

Lopez

D'Souza

et al. 2017

Diabetes Obesity Metabolism

Self Cite

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A healthy dietary pattern with a low inflammatory potential reduces the risk of gestational diabetes mellitus

et al. 2021

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Purpose An optimal diet for lowering the risk of gestational diabetes mellitus (GDM) is still to be defined, but may comprise of nutrient intakes, dietary patterns, diet quality, and eating frequency. This study was designed to investigate the contribution of diet in developing GDM in a comprehensive way. Methods The dietary intake of overweight or obese women, a risk group for GDM (n = 351), was assessed using 3-day food diaries and diet quality questionnaires in early pregnancy. Eating frequency and nutrient intakes were calculated, and dietary patterns identified using principal component analysis. The inflammatory potential of the diet was determined by calculating the dietary inflammatory index (DII®) and energy-adjusted DII (E-DII™). GDM was diagnosed with an oral glucose tolerance test at 24–28 gestational weeks. Results Higher adherence to ‘healthier dietary pattern’ characterized by consumptions of vegetables and rye bread associated with a reduced risk of GDM (adjusted OR 0.27, 95% CI 0.11–0.70). Higher E-DII score, indicating pro-inflammatory diet, was associated with a 27% higher risk of GDM (adjusted OR 1.27; 95% CI 1.08–1.49) for each E-DII point. In the evaluation of nutrient intakes, total fat, saturated fatty acids (SFAs), and trans fatty acids were higher and fiber lower in women developing GDM compared to women not developing GDM (all p < 0.05). Intakes of total fat, SFAs, and trans fatty acids were also significant predictors for GDM (all p < 0.05). Conclusions The results emphasize the importance of an overall healthy diet and limitation of foods with SFAs, and other nutrients with a high inflammatory potential in reducing the risk of GDM. Trial registration ClinicalTrials.gov Identifier: NCT01922791, August 14, 2013.

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