Relationship of dietary fat and serum cholesterol ester and phospholipid fatty acids to markers of insulin resistance in men and women with a range of glucose tolerance☆
Abstract
High-fat diets are associated with insulin resistance, however, this effect may vary depending on the type of fat consumed. The purpose of this study was to determine the relationship between intakes of specific dietary fatty acids (assessed by 3-day diet records and fatty acid composition of serum cholesterol esters [CEs] and phospholipids [PLs]) and glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Nineteen men and 19 women completed the study. Nine subjects had type 2 diabetes or impaired glucose tolerance. Fasting insulin correlated with reported intakes of total fat (r = .50, P < .01), monounsaturated fat (r = .44, P < .01), and saturated fat (r = .49, P < .01), but not with trans fatty acid intake (r = .11, not significant [NS]). Fasting glucose also correlated with total (r = .39, P < .05) and monounsaturated fat intakes (r = .37, P < .05). In multivariate analysis, both total and saturated fat intake were strong single predictors of fasting insulin (R2 .25), and a model combining dietary and anthropometric measures accounted for 47% of the variance in fasting insulin. Significant relationships were observed between fasting insulin and the serum CE enrichments of myristic (C14:0), palmitoleic (C16:1), and dihomo-γ-linolenic (C20:3n-6) acids. In multivariate analysis, a model containing CE 14:0 and percent body fat explained 45% of the variance in fasting insulin, and C14:0 and age explained 30% of the variance in fasting glucose. PL C20:3n-6 explained 30% of the variance in fasting insulin, and a model including PL C18:1n-11 cis, C20:3n-6, age and body fat had an R2 of .58. In conclusion, self-reported intake of saturated and monounsaturated fats, but not trans fatty acids, are associated with markers of insulin resistance. Furthermore, enhancement of dihomo-γ-linolenic and myristic acids in serum CE and PL, presumably markers for dietary intake, predicted insulin resistance.
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Dietary factors and gestational diabetes mellitus: An umbrella review
2023, Trends in Food Science and TechnologyAssociations between dietary factors and gestational diabetes mellitus (GDM) risk are inconsistent.
We evaluated existing meta-analyses based on prospective cohort studies or randomized controlled trials till March 2022. We determined methodological quality and evidence certainty by A Measurement Tool to Assess Systematic Reviews 2 and NutriGrade, respectively. We recalculated pooled effect estimates risk ratio (RR), corresponding 95% confidence interval (CI), and between-study heterogeneity from the primary studies, except for dose-response analyses from which data were directly extracted and evaluated.
We included 14 studies involving 27 dietary factors in this analysis. We did not observe high-certainty evidence. We found three pieces of moderate-certainty evidence for increased GDM risk: 80 g/d increments in potato consumption, high and 100 mg/d increments in cholesterol intake, high and 1.0 mg/d increments in heme iron intake; three pieces of moderate-certainty evidence for reduced GDM: myo-inositol supplement, vitamin D supplement >601 IU/d, probiotics intake >5 × 109 colony-forming units, compared with their corresponding control groups. In region-specific analysis, we found that western dietary pattern and animal meat consumption are associated with a high GDM risk in western countries, while vitamin D supplement >601 IU/d is associated with a low GDM risk in eastern countries. In meat-type analysis, we found that red meat and processed red meat consumptions are associated with high GDM risk, while poultry and fish consumption is not. In conclusion, due to the moderate-to-low certainty of evidence and the relatively large heterogeneity between studies, further high-quality investigations are needed.
Non-conventional therapeutical approaches to acne vulgaris related to its association with metabolic disorders
2022, European Journal of PharmacologyThe ever-increasing frequency of metabolic syndrome (MetS) is still a major challenge of the public health care system, worldwide. In recent years, researchers have been drawn to the uncommon (at first look) link between skin illnesses and MetS. Because of the pro-inflammatory mechanisms and insulin resistance (IR) that are upregulated in metabolic syndrome, many skin disorders are correlated to metabolic dysfunctions, including acne vulgaris. A comprehensive understanding of the link between MetS and acne vulgaris may contribute to the development of new treatment strategies. The current review focuses on dietary and therapeutic interventions and assesses the effect of various approaches such as improving diet by avoiding certain food products (i.e., milk and chocolate) or increasing the intake of others (i.e., food products rich in omega-3 fatty acids), metformin administration, therapy with plant extracts, plant essential oils, and probiotic supplementation on the improvement of certain acne vulgaris severity parameters. These therapeutic approaches, when combined with allopathic treatment, can improve the patients' quality of life.
Associations Between Erythrocyte Membrane Fatty Acid Compositions and Biomarkers of Vascular Health in Adults With Type 1 Diabetes With and Without Insulin Resistance: A Cross-Sectional Analysis
2022, Canadian Journal of DiabetesThe aim of this study was to assess the relationship between specific erythrocyte fatty acid levels and vascular health in type 1 diabetes (T1D) with and without insulin resistance (IR).
We analyzed baseline pretreatment data in a subset of 23 patients with T1D from a previously published randomized controlled trial consisting of comprehensive erythrocyte-derived fatty acid profiles and a panel of inflammation-associated endothelial markers. Estimated glucose disposal rate was used to identify and categorize patients with IR. We utilized principal component analysis (PCA) to cluster vascular biomarkers to compute a single “vascular signal” and utilized univariate linear regression models to investigate the association with IR and fatty acid profiles.
Subjects with IR displayed significantly higher levels of linoleic acid (p=0.001), lower levels of eicosapentaenoic acid (EPA) (p<0.001), lower levels of omega-3 polyunsaturated fatty acid (n-3PUFA) (p<0.006) and an increased omega-6 (n-6)PUFA:n-3PUFA ratio (p=0.001). IR was associated with significantly higher linoleic acid levels, total n-6PUFA and an increased ratio of n-6PUFA:n-3PUFA, and negatively associated with arachidonic acid and EPA levels, total saturated fatty acid and total n-3PUFA. The PCA-derived vascular biomarker cluster was positively associated with linoleic acid and n-6PUFA:n-3PUFA ratio, and inversely associated with EPA.
Specific erythrocyte membrane fatty acid compositions are associated with impaired vascular health and IR in adults with T1D. These findings suggest that IR and risk of associated complications may be influenced by specific fatty acid profiles, and thus potentially modified by the selective targeting of dietary fatty acids.
L’objectif de la présente étude était d’évaluer la relation entre les concentrations en acides gras érythrocytaires et la santé vasculaire des patients atteints du diabète de type 1 (DT1) qui présentent ou non une insulinorésistance (IR).
Nous avons analysé les données initiales, préalables au traitement, d’un sous-ensemble de 23 patients atteints du DT1 d’un essai clinique à répartition aléatoire publié précédemment, qui étaient constituées de profils des acides gras érythrocytaires complets et d’un panel de marqueurs endothéliaux associés à l’inflammation. L’estimation du débit de perfusion du glucose a été utilisée pour déterminer et classer par catégories les patients qui montraient une IR. Nous avons utilisé l’analyse en composantes principales (ACP) pour regrouper les biomarqueurs vasculaires afin d’évaluer le « signal vasculaire » isolément et utilisé les modèles de régression linéaire univariée pour examiner l’association avec l’IR et les profils des acides gras.
Les sujets qui ont montré une IR affichaient des concentrations significativement plus élevées en acide linoléique (p = 0,001), des concentrations plus faibles en acide eicosapentaénoïque (AEP) (p < 0,001), des concentrations totales plus faibles en acides gras polyinsaturés oméga-3 (AGPI n-3) (p < 0,006) et une augmentation du ratio AGPI n-6 :AGPI n-3 (p=0,001). L’IR a été associée à des concentrations significativement plus élevées en acide linoléique, les AGPI n-6 totaux, et à un ratio AGPI n-6 :AGPI n-3 accru, et associée de façon négative à des concentrations en acide arachidonique et en AEP, en acides gras saturés totaux et en AGPI n-3 totaux. Le regroupement des biomarqueurs vasculaires issus de l’ACP était associé de façon positive à l’acide linoléique et au ratio AGPI n-6 :AGPI n-3, et associé de façon inverse à l’AEP.
Les teneurs en acides gras spécifiques des membranes érythrocytaires sont associées à une détérioration de la santé vasculaire et de l’IR chez les adultes atteints du DT1. Ces résultats montrent que l’IR et le risque de complications associées peuvent être influencés par les profils des acides gras spécifiques et, par conséquent, être potentiellement modifiés par la sélection judicieuse des acides gras alimentaires.
The snapshot of metabolic health in evaluating micronutrient status, the risk of infection and clinical outcome of COVID-19
2021, Clinical Nutrition ESPENCOVID-19 has re-established the significance of analyzing the organism through a metabolic perspective to uncover the dynamic interconnections within the biological systems. The role of micronutrient status and metabolic health emerge as pivotal in COVID-19 pathogenesis and the immune system's response. Metabolic disruption, proceeding from modifiable factors, has been proposed as a significant risk factor accounting for infection susceptibility, disease severity and risk for post-COVID complications. Metabolomics, the comprehensive study and quantification of intermediates and products of metabolism, is a rapidly evolving field and a novel tool in biomarker discovery. In this article, we propose that leveraging insulin resistance biomarkers along with biomarkers of micronutrient deficiencies, will allow for a diagnostic window and provide functional therapeutic targets. Specifically, metabolomics can be applied as: a. At-home test to assess the risk of infection and propose nutritional support, b. A screening tool for high-risk COVID-19 patients to develop serious illness during hospital admission and prioritize medical support, c(i). A tool to match nutritional support with specific nutrient requirements for mildly ill patients to reduce the risk for hospitalization, and c(ii). for critically ill patients to reduce recovery time and risk of post-COVID complications, d. At-home test to monitor metabolic health and reduce post-COVID symptomatology. Metabolic rewiring offers potential virtues towards disease prevention, dissection of high-risk patients, taking actionable therapeutic measures, as well as shielding against post-COVID syndrome.
Trans fatty acids and mortality
2018, The Molecular Nutrition of FatsThe term “trans fatty acids” (TFAs) describes unsaturated fatty acids that contain at least one double bond in trans configuration. Ruminant animals produce TFAs in small quantities. Industrial hardening produces far larger amounts of TFAs. A high intake of TFAs has been associated with an increased risk of cardiovascular disease. Legal actions to limit the use of TFA are effective as demonstrated by markedly decreasing levels of TFA in most nations worldwide. Although there is a broad consent that the consumption of high amounts of industrially produced TFAs is harmful for human health and leads to a higher mortality risk, the picture is less clear regarding a low intake with a majority of studies reporting no association with LDL-C or cardiovascular risk. Regarding ruminant-derived TFAs, most studies do not observe an increased mortality risk and some beneficial effects on glucose metabolism and diabetes incidence have been reported.
Oleate dose-dependently regulates palmitate metabolism and insulin signaling in C2C12 myotubes
2016, Biochimica et Biophysica Acta - Molecular and Cell Biology of LipidsBecause the protective effect of oleate against palmitate-induced insulin resistance may be lessened in skeletal muscle once cell metabolism is overloaded by fatty acids (FAs), we examined the impact of varying amounts of oleate on palmitate metabolic channeling and insulin signaling in C2C12 myotubes. Cells were exposed to 0.5 mM of palmitate and to increasing doses of oleate (0.05, 0.25 and 0.5 mM). Impacts of FA treatments on radio-labelled FA fluxes, on cellular content in diacylglycerols (DAG), triacylglycerols (TAG), ceramides, acylcarnitines, on PKCθ, MAPKs (ERK1/2, p38) and NF-ΚB activation, and on insulin-dependent Akt phosphorylation were examined.
Low dose of oleate (0.05 mM) was sufficient to improve palmitate complete oxidation to CO2 (+ 29%, P < 0.05) and to alter the cellular acylcarnitine profile. Insulin-induced Akt phosphorylation was 48% higher in that condition vs. palmitate alone (p < 0.01). Although DAG and ceramide contents were significantly decreased with 0.05 mM of oleate vs. palmitate alone (− 47 and − 28%, respectively, p < 0.01), 0.25 mM of oleate was required to decrease p38 MAPK and PKCθ phosphorylation, thus further improving the insulin signaling (+ 32%, p < 0.05). By contrast, increasing oleate concentration from 0.25 to 0.5 mM, thus increasing total amount of FA from 0.75 to 1 mM, deteriorated the insulin signaling pathway (− 30%, p < 0.01). This was observed despite low contents in DAG and ceramides, and enhanced palmitate incorporation into TAG (+ 27%, p < 0.05). This was associated with increased incomplete FA β-oxidation and impairment of acylcarnitine profile. In conclusion, these combined data place mitochondrial β-oxidation at the center of the regulation of muscle insulin sensitivity, besides p38 MAPK and PKCθ.
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Supported by US Department of Agriculture Grant No. 96034323-3031 (to G.A.B.).