Fatty Acids, Obesity, and Insulin Resistance: Time for a Reevaluation
- 1Oxford Centre for Diabetes, Endocrinology and Metabolism, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, U.K.
- 2National Institute for Health Research, Oxford Biomedical Research Centre, Oxford Radcliffe Hospitals Trust, Oxford, U.K.
- Corresponding author: Fredrik Karpe, fredrik.karpe{at}ocdem.ox.ac.uk.
Article Figures & Tables
Figures
- FIG. 1.
Bubble graph representing the relationship between the difference in estimated fat mass and the difference in plasma NEFA concentration in 43 independent publications published 1990–2008 (Supplementary Table 1) between lean and overweight/obese subjects. Each bubble represents one study, and the bubble area is proportional to the number of observations (participants).
- FIG. 2.
Relationships between plasma NEFA concentrations and BMI in two cohorts. Black bars, plasma NEFA concentrations; gray bars, fat mass. A: Data from the Paris Prospective Study (46), courtesy of Beverley Balkau, in 5,790 individuals. Fat mass has been estimated from BMI (61). B: Data from OBB for 1,591 individuals. In each case, the mean ± SE plasma NEFA concentration is shown for quintiles of BMI. The BMI quintiles were as follows: I: <22.5 kg/m2; II: 22.5–24.4 kg/m2; III: 24.4–26.4 kg/m2; IV: 26.4–29.2 kg/m2; V: >29.2 kg/m2.
- FIG. 3.
Relationships between NEFA release from subcutaneous abdominal adipose tissue and fat mass (A) and fasting insulin (B) in different groups of subjects. The NEFA release has been quantified with the same technique in separate group of subjects from previous studies in our laboratory using arteriovenous concentration differences across abdominal subcutaneous tissue multiplied by the tissue blood flow. Only data from men are shown. Open circle, healthy lean control subjects; solid circle, healthy obese subjects (62). Solid square, lean control subjects (80). Upward triangle, lean control subjects (81). Cross, lean control subjects (82). Square with hour-glass fill: healthy control subjects aged 31–59 years, BMI 22–28 kg/m2 (K. Manolopoulos, unpublished data). Open star, control subjects for insulin resistance study; solid star, men with insulin resistance (83). Downward triangle, healthy obese men (12). Open diamond, type 2 diabetic patients on rosiglitazone; solid diamond, same patients on placebo (84). Note that the different groups of lean control subjects had different characteristics (age, BMI) as detailed in the individual publications. For each group, mean values ± SE are shown.
Tables
- TABLE 1
Univariate relationships (Spearman’s rank correlation coefficient) with plasma NEFA concentrations in the Oxford BioBank
NEFA with BMI Fat mass WHR Insulin HOMA-IR TG 3-OHB CRP SBP DBP Males rs 0.057 0.031 0.034 −0.028 −0.025 0.017 0.570 0.045 0.157 0.050 P 0.094 0.362 0.323 0.409 0.466 0.616 <0.001 0.264 <0.001 0.141 n 859 859 856 859 859 859 857 627 859 859 Females rs 0.091 0.081 0.043 0.086 0.094 0.142 0.654 0.116 0.132 0.126 P 0.007 0.017 0.209 0.012 0.006 < 0.001 <0.001 0.004 <0.001 <0.001 n 861 861 859 861 861 861 861 633 861 861 Samples were from 1,720 healthy individuals, median age 41 (range 2–53) years, median BMI 25 (range 15–48) kg/m2. 3-OHB, 3-hydroxybutyrate; DBP, diastolic blood pressure; HOMA-IR, homeostatic model assessment of insulin resistance; SBP, systolic blood pressure; WHR, waist-to-hip ratio.
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- Article
- FATTY ACIDS AND METABOLIC PHYSIOLOGY
- FATTY ACIDS AND PATHOPHYSIOLOGY
- NEFA CONCENTRATIONS IN OBESITY: SYSTEMATIC LITERATURE REVIEW
- NEFA CONCENTRATIONS IN GROUPS FROM A RANDOM NONDIABETIC POPULATION SAMPLE
- FASTING NEFA RELEASE IN RELATION TO FAT MASS OR FASTING INSULIN
- NONFASTING NEFA CONCENTRATIONS
- SUMMARY AND CONCLUSIONS
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