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Journal of the American College of Nutrition, Vol. 26, No. 4, 321-326 (2007)
Published by the American College of Nutrition

Body Fat Distribution and Insulin Resistance: Beyond Obesity in Nonalcoholic Fatty Liver Disease among Overweight Men

Seung Ha Park, MD, Byung Ik Kim, MD, Sang Hoon Kim, MD, Hong Joo Kim, MD, Dong Il Park, MD, Yong Kyun Cho, MD, In Kyung Sung, MD, Chong Il Sohn, MD, Hyang Kim, MD, Dong Keuk Keum, MD, Heung Dae Kim, MD, Jung Ho Park, MD, Jin Ho Kang, MD and Woo Kyu Jeon, MD

Division of Gastroenterology (S.H.P., B.I.K., S.H.K., H.J.K., D.I.P., Y.K.C., C.I.S., H.K., J.H.P., J.H.K., W.K.J.)
Department of Internal Medicine and Laboratory Medicine (D.K.K.)
Department of General Surgery (H.D.K.), Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine
Department of Internal Medicine, Konkuk University Hospital, Konkuk University School of Medicine (I.K.S.), Seoul, KOREA

Address reprint requests to: Byung Ik Kim, M.D., Division of Gastroenterology, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University, School of Medicine, 108, Pyung-Dong, Jongro-Ku, Seoul, 110-746, KOREA. E-mail: bik.kim{at}samsung.com


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Objective: The aim of this study was to characterize the relationship between nonalcoholic fatty liver disease (NAFLD) and body fat distribution and insulin resistance in a sample of non-diabetic overweight men.

Subjects and Methods: We conducted a cross-sectional survey of 117 overweight men with NAFLD, as well as 117 controls, who were matched with regard to age and body mass index. None of the study subjects exhibited signs of alcohol abuse, hepatitis B or C, diabetes or fasting hyperglycemia, or hypertension. The diagnosis of NAFLD was based on dual findings of elevated alanine aminotransferase levels and sonographically-determined fatty liver. Body fat distribution was assessed via bioelectrical impedance. Insulin resistance was evaluated via homeostasis model assessment (HOMA-IR).

Results: The risk of developing NAFLD was found to be profoundly associated with elevated measurements of waist circumference, fat mass, percentage of body fat and abdominal fat, iron, triglycerides, apolipoprotein B, and results of HOMA-IR. Multivariate analysis revealed that NAFLD was significantly associated with elevated measurements of waist circumference, iron, apolipoprotein B, and HOMA-IR.

Conclusions: Our study provides evidence for a profound and dose-dependent association of NAFLD with central adiposity, insulin resistance in overweight men lacking complications of metabolic syndrome. Overweight subjects with insulin resistance or central adiposity were at more risk of NAFLD than were those subjects with less insulin resistance or central adiposity, even those with a similar degree of obesity.

Key words: nonalcoholic fatty liver disease, central adiposity, insulin resistance


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Nonalcoholic fatty liver disease (NAFLD) is a common liver disorder, which is frequently identified in individuals in the absence of significant alcohol consumption. Although a number of circumstances have been implicated as risk factors, obesity is clearly the principal risk factor for the development of NAFLD [1]. It is believed that the prevalence of NAFLD is increasing, along with increasing obesity. The prevalence of NAFLD among obese subjects has been reported in a variety of studies, according to its definition. Using sonographic surveys in obese subjects, the prevalence of NAFLD has been documented at 57.5%–60% in the East [2,3], and 75.8% in the West [4]. On the other hand, the prevalence of the combination of sonographic fatty liver and elevated aminotransferase among the obese has been estimated to be approximately 20% [5]. Despite the absolute certainty of the relationship between obesity and NAFLD, all obese individuals do not necessarily develop NAFLD. In addition, central adiposity appears to be a more powerful predictor than does simple obesity [6,7].

The existence of an association between obesity and insulin resistance has been theorized on many occasions, and insulin resistance is also considered to be a primary risk factor for NAFLD [8,9]. Although obesity is generally regarded as the principal cause of insulin resistance, not all obese people develop this condition. According to the European Group for the Study of Insulin Resistance, only 26% of obese individuals exhibit insulin resistance [10]. Furthermore, insulin resistance, at any given degree of obesity, exacerbates the risk of coronary heart disease and type 2 diabetes, sharing the risk factors of NAFLD [11].

We extended the hypothesis that obese people with insulin resistance and central adiposity are at more risk of NAFLD than are those subjects with lesser degrees of insulin resistance and central adiposity, even with a similar degree of obesity. Thus, the objective of this study was to characterize the relationship between NAFLD and body fat distribution and insulin resistance in non-diabetic and normotensive overweight men.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects
Our cross-sectional study was performed using data obtained from 3,530 men, all of whom were older than 20 years of age, and had undergone health screenings at the Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, from January to December, 2003. This study was approved by the Institutional Review Board of the Kangbuk Samsung Hospital, and informed consent was provided by all participants. Of the 3,530 participants, 416 men exhibited the combination of sonographic fatty liver and elevated alanine aminotransferase levels (≥40 IU/L). Of these 416 men, 134 heavy drinkers (>30g/day), 9 with hepatitis B, and 2 with hepatitis C were excluded from this study. 271 of the remaining subjects were finally diagnosed as NAFLD.

Of the 271 men with NAFLD, 154 were excluded from the study due to the following exclusion criteria: non-overweight (body mass index <25 kg/m2, n = 57), previous history of coronary heart disease (n = 9), previous history of diabetes or fasting hyperglycemia (≥110 mg/dL, n = 29), previous history of hypertension or high blood pressure (≥140/90 mmHg, n = 30), use of lipid-lowering agents (n = 9), or current medications (n = 20). The remaining 117 men with NAFLD were included in this study. We selected 117 men as control subjects, so that the distribution of the ages and body mass indices of the controls would be as similar as possible to the distribution in the subjects with NAFLD. The control subjects were also required to fulfill the above-mentioned inclusion and exclusion criteria for NAFLD patients, including normal liver function tests and negative sonography for hepatic fat.

Histories of alcohol consumption were assessed according to the type of alcoholic beverage consumed, the frequency of alcohol consumption per week, and the amount drunk per day. Subjects consuming less than 30g of alcohol per day were considered to be non-drinkers [12,13]. The diagnosis of sonographic fatty liver was established according to the combination of liver-kidney contrast (bright liver) with vascular blurring, using a 3.5 MHz probe (Logic Q700 MR, GE, Milwaukee, WI, USA) [14].

Methods
The index of insulin resistance used in our calculations was derived from the homeostasis model assessment (HOMA-IR), and was computed according to the following formula: (fasting insulin in µU/ml x fasting glucose in mmol/L)/22.5 [15]. Body mass indices (kg/m2) were calculated according to objective body weight and height measurements. Subjects with a body mass index of 25 or above were considered to be overweight according to WHO criteria [16]. Body fat distribution was assessed with an eight polar bioelectrical impedance (InBody 3.0, Biospace, Seoul, Korea), which was validated with regard to reproducibility and accuracy for body composition [17,18]. The mean blood pressure was selected from 2 measurements, taken with the subject in a supine position.

Fasting blood sugar was measured by the hexokinase method, after 12 hours of fasting, followed by measurements of total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol (Advia 1650, Bayer, Fernwald, Germany). Apolipoprotein A-I and Apolipoprotein B were measured via rate nephelometry (IMMAGE System, Beckman Coulter, California, USA). Insulin (Biosource, Belgium) was assayed via immunoradiometric assays. We detected no cross-reactivity with proinsulin. The intraassay variation coefficients were 2.1–4.5%, and the interassay variation coefficients for the quality controls were 4.7–12.2%. C-reactive protein levels were assayed by particle-enhanced immunonephelometry, using a BNTM System (N High Sensitivity CRP, Dade Behring, Marburg, Germany).

Statistical Analysis
Differences between mean values in the control and case subjects were tested by Student’s t-tests. The Odds ratio (OR) and 95% confidence intervals (CIs) for the NAFLD risk factors were calculated via the standard logistic regression model, using SPSS software (Version 11.0, Inc., Chicago, IL) for MS Windows. During the logistic regression analysis, continuous variables were categorized according to their standard deviation values. Multivariate analysis was performed on the basis of the univariate analyses. Due to the skewness of the triglycerides, C-reactive protein, HOMA-IR, and liver enzymes, their values were logarithmically transformed for analysis. The level of significance was set at 5% for all performed tests.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
ACKNOWLEDGMENTS
 REFERENCES
 
The clinical and metabolic characteristics of the 117 NAFLD subjects and 117 controls are presented in Table 1. We detected no significant differences with regard to age, body mass index, and amount of alcohol consumption between the two groups. The NAFLD group exhibited significantly higher values for waist circumference, body fat indices, liver enzymes, fasting insulin, triglycerides, apolipoprotein B, and HOMA-IR than the control group.


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  		Table 1. Characteristics of the Study Population

 
The risk of developing NAFLD was found to be significantly associated with elevated measurements of waist circumference, body fat indices, iron, triglycerides, apolipoprotein B, and HOMA-IR (Table 2). Logistic regression model was used to carry out multivariate analysis, which was, in turn, carried out on the basis of the results of univariate analysis. This result indicated that NAFLD was significantly associated with elevated measurements of waist circumference, iron, apolipoprotein B, and HOMA-IR, (Table 3).


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  		Table 2. Univariate Relationship between Risk Factors and Nonalcoholic Fatty Liver Disease

 

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  		Table 3. Multivariate Relationship between Risk Factors and Nonalcoholic Fatty Liver Disease

 

   DISCUSSION
 
This study is a cross-sectional study to assess a broad range of NAFLD risk factors in seemingly-healthy overweight men lacking complications of metabolic syndrome, including a previous history of diabetes or hypertension, fasting hyperglycemia, high blood pressure, or current treatment with medications. While the design of current study is to identify nutritional risk factors of NAFLD in the group without complication of metabolic syndrome, further study aimed at reducing the apparent prevalence of NAFLD in overweight men is warranted. In this study, those with significant alcohol consumption or viral hepatitis are excluded. However, it should be noted that liver damage is potentiated by interactions of alcohol, hepatic virus, and features of the metabolic syndrome [19,20].

We decided to predicate the diagnosis of NAFLD on a combination of elevated alanine aminotransferase and the sonographic diagnosis of fatty liver as the study end point. We did this in order to characterize the relevant risk factors, with the aim of developing strategies for risk stratification in overweight men. This end point, though, has some limitations, as radiological imaging is insensitive to steatosis of less than 30%, and also lacks sensitivity with regard to identification of the severity of the condition [21]. Also, liver enzymes are not considered to be sensitive or specific for diagnosing NAFLD, and a significant number of NAFLD patients may have normal liver enzymes. The accuracy of the combination of elevated liver enzymes and radiographic techniques, as a surrogate for the detection of fatty liver disease, need to be evaluated.

Although obesity is classically the factor which is most strongly associated with NAFLD, the possibility remains that the higher risk for NAFLD observed among obese individuals can be attributed to conditions which frequently coexist with overweight, including diabetes, hyperlipidemia, or hypertension. Thus, we attempted to strictly evaluate the effects of insulin resistance on NAFLD, by excluding any factors which might serve to influence insulin resistance. This study indicates a profound and dose-dependent association between NAFLD and increasing insulin resistance, which is consistent with the results of previous studies [22–25]. This result suggests that overweight insulin-resistant individuals are at a greater risk of NAFLD than are insulin-sensitive subjects with similar degrees of obesity. Currently, the mechanisms underlying the observed association of insulin resistance with NAFLD remains poorly understood. It can be assumed that excess portal adipose tissue increases the influx of free fatty acids through the portal vein to the liver, possibly resulting in the accumulation of hepatic fat [26]. Insulin resistance is the basis of hepatic steatosis, and that fat-accumulated hepatocytes are predisposed to injury by endotoxins or other oxidative stresses [27]. However, screening methods for insulin resistance, and the definition of insulin resistance, have not, thus far, been established in clinical practice. With regard to insulin resistance, the recent report of the Adult Treatment Panel III has formulated criteria for the diagnosis of metabolic syndrome [28]. Although these criteria have low sensitivity with regard to the identification of insulin-resistant subjects [29,30], these criteria have, in part, been devised to obviate the need for direct insulin-resistance measures, and may provide a surrogate for insulin resistance in clinical practice. Recent two studies based on histological verification indicate that the over 85% of patients with nonalcoholic steatohepatitis, and approximately 55% of simple steatosis suffer from metabolic syndrome, and the presence of metabolic syndrome is associated with potentially progressive and severe liver disease [25,31].

This study also reveals that waist circumference as a measure of central obesity is a risk factor which is independent of overall obesity as indicated by body mass index and body fat mass. It now appears that central adiposity may be at least as important as obesity in terms of the development of hepatic steatosis. Three population-based, epidemiological studies have concluded that elevated alanine aminotransferase activity is profoundly and independently associated with abdominal height, waist circumference, and the ratio of waist-to-hip circumference [6,32,33]. In addition, central adiposity has been demonstrated to be associated with sonographic fatty liver, as well as degree of steatosis, upon liver biopsy [7,24,34].

Previous evidence concerning the relationship between serum iron and NAFLD remains controversial. This study reveals that serum iron is associated with NAFLD. This result was corroborated by a large population-based study, which determined that elevated alanine aminotransferase activity was positively associated with increasing serum iron concentrations [35]. In a case-control study, contrary to our findings, iron overload indices appeared not to constitute an independent determinant for NAFLD [36]. In conclusion, our study provides evidence for a profound and dose-dependent association of NAFLD with central adiposity and insulin resistance in overweight men lacking confounding factors. The relationship between traditional risk factors, including obesity, diabetes, and hyperlipidemia, with NAFLD, can be attributed primarily to its association with central adiposity and insulin resistance. Overweight people suffering from insulin resistance or central adiposity are more at risk for NAFLD than are those subjects with lesser degrees of insulin resistance or central adiposity, even those exhibiting similar degrees of obesity.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 ACKNOWLEDGMENTS
REFERENCES
 
This study was supported by a grant from the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (No. A050021).

Received February 16, 2005. Accepted February 6, 2007.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 ACKNOWLEDGMENTS
 REFERENCES
 

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