Relationships between Composition of Major Fatty Acids and Fat Distribution and Insulin Resistance in Japanese

Objective. The aim of this study was to evaluate the relationships between the composition of free fatty acids (FFAs) and metabolic parameters, including body fat distribution, in Japanese.Methods. The study subjects were 111 Japanese patients (54 males, 57 females). Metabolic parameters and visceral and subcutaneous fat areas as determined by CT scanning at the umbilical level were measured. Glucose tolerance test (GTT) was performed by administering 75 g glucose orally.Results. The percentage of linoleic acid (C18:2), the greatest constituent among FFAs, was negatively correlated with visceral fat area (r=−0.411,p<0.0001), fasting glucose (r=−0.330,p<0.0001), HbA1c (r=−0.231,p=0.0146), and systolic blood pressure (r=−0.224,p=0.0184). Linoleic acid percentage was also significantly negatively correlated with HOMA-IR (r=−0.416,p<0.0001) by simple correlation. Based on the findings of OGTT, the 111 subjects were classified into three groups: 33 with normal glucose tolerance, 71 with impaired glucose tolerance (IGT), and 7 diabetic subjects. The percentage of serum linoleic acid in diabetic subjects was significantly lower than that in normal subjects.Conclusion. We conclude that serum linoleic acid level is negatively correlated with the accumulation of visceral fat in relation to a reduction of insulin resistance in Japanese subjects.

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Effect of Pioglitazone on Abdominal Fat Distribution and Insulin Sensitivity in Type 2 Diabetic Patients

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jcem.87.6.8567 ◽

2002 ◽

Vol 87 (6) ◽

pp. 2784-2791 ◽

Cited By ~ 322

Author(s):

Yoshinori Miyazaki ◽

Archana Mahankali ◽

Masafumi Matsuda ◽

Srikanth Mahankali ◽

Jean Hardies ◽

...

Keyword(s):

Insulin Resistance ◽

Visceral Fat ◽

Fat Distribution ◽

Abdominal Fat ◽

Hepatic Insulin Resistance ◽

Diabetic Patients ◽

Visceral Fat Area ◽

Insulin Clamp ◽

Pioglitazone Treatment

We examined the effect of pioglitazone on abdominal fat distribution to elucidate the mechanisms via which pioglitazone improves insulin resistance in patients with type 2 diabetes mellitus. Thirteen type 2 diabetic patients (nine men and four women; age, 52 ± 3 yr; body mass index, 29.0 ± 1.1 kg/m2), who were being treated with a stable dose of sulfonylurea (n = 7) or with diet alone (n = 6), received pioglitazone (45 mg/d) for 16 wk. Before and after pioglitazone treatment, subjects underwent a 75-g oral glucose tolerance test (OGTT) and two-step euglycemic insulin clamp (insulin infusion rates, 40 and 160 mU/m2·min) with [3H]glucose. Abdominal fat distribution was evaluated using magnetic resonance imaging at L4–5. After 16 wk of pioglitazone treatment, fasting plasma glucose (179 ± 10 to 140 ± 10 mg/dl; P < 0.01), mean plasma glucose during OGTT (295 ± 13 to 233 ± 14 mg/dl; P < 0.01), and hemoglobin A1c (8.6 ± 0.4% to 7.2 ± 0.5%; P < 0.01) decreased without a change in fasting or post-OGTT insulin levels. Fasting plasma FFA (674 ± 38 to 569 ± 31 μEq/liter; P < 0.05) and mean plasma FFA (539 ± 20 to 396 ± 29 μEq/liter; P < 0.01) during OGTT decreased after pioglitazone. In the postabsorptive state, hepatic insulin resistance [basal endogenous glucose production (EGP) × basal plasma insulin concentration] decreased from 41 ± 7 to 25 ± 3 mg/kg fat-free mass (FFM)·min × μU/ml; P < 0.05) and suppression of EGP during the first insulin clamp step (1.1 ± 0.1 to 0.6 ± 0.2 mg/kg FFM·min; P < 0.05) improved after pioglitazone treatment. The total body glucose MCR during the first and second insulin clamp steps increased after pioglitazone treatment [first MCR, 3.5 ± 0.5 to 4.4 ± 0.4 ml/kg FFM·min (P < 0.05); second MCR, 8.7 ± 1.0 to 11.3 ± 1.1 ml/kg FFM·min (P < 0.01)]. The improvement in hepatic and peripheral tissue insulin sensitivity occurred despite increases in body weight (82 ± 4 to 85 ± 4 kg; P < 0.05) and fat mass (27 ± 2 to 30 ± 3 kg; P < 0.05). After pioglitazone treatment, sc fat area at L4–5 (301 ± 44 to 342 ± 44 cm2; P < 0.01) increased, whereas visceral fat area at L4–5 (144 ± 13 to 131 ± 16 cm2; P < 0.05) and the ratio of visceral to sc fat (0.59 ± 0.08 to 0.44 ± 0.06; P < 0.01) decreased. In the postabsorptive state hepatic insulin resistance (basal EGP × basal immunoreactive insulin) correlated positively with visceral fat area (r = 0.55; P < 0.01). The glucose MCRs during the first (r = −0.45; P < 0.05) and second (r = −0.44; P < 0.05) insulin clamp steps were negatively correlated with the visceral fat area. These results demonstrate that a shift of fat distribution from visceral to sc adipose depots after pioglitazone treatment is associated with improvements in hepatic and peripheral tissue sensitivity to insulin.

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Visceral fat and insulin resistance — causative or correlative?

British Journal Of Nutrition ◽

10.1017/s0007114500000982 ◽

2000 ◽

Vol 83 (S1) ◽

pp. S71-S77 ◽

Cited By ~ 261

Author(s):

Keith N. Frayn

Keyword(s):

Insulin Resistance ◽

Fatty Acids ◽

Portal Vein ◽

Visceral Fat ◽

Subcutaneous Fat ◽

Causal Link ◽

Abdominal Fat ◽

High Rate ◽

Fat Accumulation ◽

Visceral Fat Accumulation

The association between abdominal fat accumulation and risk of chronic diseases, including type II diabetes and coronary heart disease, has long been recognized. Insulin resistance may be a key factor in this link. Many studies have pointed to an association between insulin resistance and intra-abdominal fat accumulation (visceral obesity). However there is no clear proof of a causal link between visceral fat accumulation and insulin resistance. In assessing the probability of a causal link, it is useful to consider potential mechanisms. One such potential causal link is the release of non-esterified fatty acids from visceral fat into the portal vein, so that they have direct effects on hepatic metabolism. Visceral fat has been shown in many studies to exhibit a high rate of lipolysis compared with subcutaneous fat depots. However, if the idea that visceral fat releases fatty acids into the portal vein at a high rate is examined critically, a number of difficulties appear. Not least of these is the fact that continued high rates of lipolysis should lead to the disappearance of the visceral fat depot, unless these high rates of fat mobilization are matched by high rates of fat deposition. There is far less evidence for high rates of fat deposition in visceral adipose tissue, and some contrary evidence. Evidence for high rates of visceral lipolysis in vivo from studies involving catheterization of the portal vein is not strong. If this potential link is discounted, then other reasons for the relationship between visceral fat and insulin resistance must be considered. One is that there is no direct causal link, but both co-correlate with some other variable. A possibility is that this other variable is subcutaneous abdominal fat, which usually outweighs intra-abdominal fat several-fold. Subcutaneous fat probably plays the major role in determining systemic plasma non-esterified fatty acid concentrations, which are relevant in determining insulin resistance. In conclusion, there is at present no proof of a causal link between visceral fat accumulation and insulin resistance, or the associated metabolic syndrome. The possibility of co-correlation with some other factor, such as subcutaneous abdominal fat accumulation, must not be forgotten.

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Visceral fat obesity is the key risk factor for the development of reflux erosive esophagitis in 40–69-years subjects

Esophagus ◽

10.1007/s10388-021-00859-5 ◽

2021 ◽

Author(s):

Shinya Ohashi ◽

Takahisa Maruno ◽

Keita Fukuyama ◽

Osamu Kikuchi ◽

Tomohiko Sunami ◽

...

Keyword(s):

Risk Factor ◽

Visceral Fat ◽

Subcutaneous Fat ◽

Erosive Esophagitis ◽

Smoking History ◽

Related Factors ◽

Visceral Fat Area ◽

Daily Alcohol Intake ◽

Gastrointestinal Reflux ◽

Total Fat

Abstract Background Visceral fat obesity can be defined quantitatively by abdominal computed tomography, however, the usefulness of measuring visceral fat area to assess the etiology of gastrointestinal reflux disease has not been fully elucidated. Methods A total of 433 healthy subjects aged 40–69 years (234 men, 199 women) were included in the study. The relationship between obesity-related factors (total fat area, visceral fat area, subcutaneous fat area, waist circumference, and body mass index) and the incidence of reflux erosive esophagitis was investigated. Lifestyle factors and stomach conditions relevant to the onset of erosive esophagitis were also analyzed. Results The prevalence of reflux erosive esophagitis was 27.2% (118/433; 106 men, 12 women). Visceral fat area was higher in subjects with erosive esophagitis than in those without (116.6 cm2 vs. 64.9 cm2, respectively). The incidence of erosive esophagitis was higher in subjects with visceral fat obesity (visceral fat area ≥ 100 cm2) than in those without (61.2% vs. 12.8%, respectively). Visceral fat obesity had the highest odds ratio (OR) among obesity-related factors. Multivariate analysis showed that visceral fat area was associated with the incidence of erosive esophagitis (OR = 2.18), indicating that it is an independent risk factor for erosive esophagitis. In addition, daily alcohol intake (OR = 1.54), gastric atrophy open type (OR = 0.29), and never-smoking history (OR = 0.49) were also independently associated with the development of erosive esophagitis. Conclusions Visceral fat obesity is the key risk factor for the development of reflux erosive esophagitis in subjects aged 40–69 years.

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Cut-Off Points of Visceral Fat Area Associated with the Risk of Insulin Resistance in Pediatric Practice

Metabolism ◽

10.1016/j.metabol.2020.154613 ◽

2021 ◽

Vol 116 ◽

pp. 154613

Author(s):

Daria Podchinenova ◽

Julia Samoilova ◽

Oxana Oleynik ◽

Maria Matveeva

Keyword(s):

Insulin Resistance ◽

Visceral Fat ◽

Pediatric Practice ◽

Visceral Fat Area

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Hepatic steatosis in Cushing's syndrome: a radiological assessment using computed tomography

Acta Endocrinologica ◽

10.1530/eje.0.1490543 ◽

2003 ◽

Vol 149 (6) ◽

pp. 543-548 ◽

Cited By ~ 91

Author(s):

AG Rockall ◽

SA Sohaib ◽

D Evans ◽

G Kaltsas ◽

AM Isidori ◽

...

Keyword(s):

Computed Tomography ◽

Hepatic Steatosis ◽

Cushing’S Syndrome ◽

Negative Correlation ◽

Visceral Fat ◽

Subcutaneous Fat ◽

Significant Negative Correlation ◽

Cushing's Syndrome ◽

Abdominal Fat ◽

Visceral Fat Area

OBJECTIVE: Hepatic steatosis may occur in association with insulin resistance and obesity, two features commonly seen in Cushing's syndrome (CS). The aim of this report is to assess the prevalence of hepatic steatosis in patients with active CS using computed tomography (CT) and to identify any associations between hepatic steatosis, endocrine and biochemical variables and body fat distribution. PATIENTS AND MEASUREMENTS: We identified 50 patients with active CS in whom appropriate CT was available to allow measurement of liver and spleen attenuation. In 26 patients, abdominal fat measurements were also available. Serum markers of CS and liver function tests were recorded. RESULTS: Ten of 50 patients had a liver-to-spleen CT attenuation ratio (L/S) of less than 1, indicating hepatic steatosis. There was a significant negative correlation between both liver attenuation and L/S ratio with total abdominal fat area, visceral fat area, the percentage of visceral fat and the visceral to subcutaneous fat ratio; the strongest negative correlation was found between visceral fat area and L/S ratio (r=-0.638, P<0.001, n=26). L/S ratio positively correlated with alkaline phosphatase levels (r=+0.423, P=0.044, n=23) but with no other serum marker of CS activity or liver enzyme. CONCLUSIONS: We have demonstrated hepatic steatosis on CT in 20% of patients with active CS. The presence of hepatic steatosis was significantly correlated with total abdominal fat area and visceral fat area.

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