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From the Clinical Research Centers |
The Center for Human Nutrition (N.A., S.M.G., A.G.), and the Department of Internal Medicine (M.C., N.A., S.M.G., A.G.), University of Texas Southwestern Medical Center, and the Department of Veteran Affairs Medical Center (M.C., S.M.G., A.G.), Dallas, Texas 75235
Address all correspondence and requests for reprints to: Nicola Abate, M.D., Department of Internal Medicine, Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235-9052. E-mail: nabate{at}mednet.swmed.edu
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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One factor contributing to insulin resistance is obesity. Very obese persons are almost uniformly insulin resistant (21, 22, 23). Asian Indians, however, rarely have marked obesity; nonetheless, they have been reported to have insulin resistance in the urban setting with only mild obesity (10, 11, 12, 13, 14). Urban habits, their accompanying mild obesity, and limited physical activity may be enough to induce insulin resistance in this population. Moreover, studies in Caucasians reveal that even a moderate degree of obesity can elicit insulin resistance when fat is accumulated predominantly in the trunk (24, 25, 26, 27, 28). Truncal obesity can be identified clinically by an increase in waist circumference or an increase in truncal skinfold thickness. Individuals with abnormal fat distribution, characterized by a high waist to hip circumference ratio or a high truncal to peripheral skinfold thickness ratio appear to be predisposed to developing insulin resistance (29). The mechanistic basis of the association between truncal obesity and insulin resistance is unknown. Some data, nonetheless, suggest that Asian Indians are susceptible to developing truncal obesity, which might account for their propensity to insulin resistance. The present study was carried out to address three questions. 1) Are Asian Indian men more insulin resistant than Caucasian men matched for total body fat content? 2) If so, are Asian Indian men more prone to predominantly truncal obesity fat distribution than are Caucasian men? 3) Does insulin resistance occur independently of obesity in Asian Indians?
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Two groups of men participated in this study: 23 were Caucasians of European ancestry and 21 were Asian Indians from the Indian subcontinent, temporarily living in the United States. They were recruited for this study by public advertisement. The study was approved by the institutional review board of the University of Texas Southwestern Medical Center (Dallas. TX). Volunteers were interviewed and screened for hematological and blood chemistry abnormalities. Subjects with diabetes mellitus and other endocrine disorders, coronary artery disease, liver function tests abnormalities, and those receiving any form of therapy were excluded. All subjects were weight stable before entering the study. After obtaining written informed consent, the study subjects were admitted for 3 days to the General Clinical Research Center of the University of Texas Southwestern Medical Center. All subjects were provided with an isocaloric diet (calculated from height, weight, and age) during the hospitalization period.
Methods
Oral glucose tolerance tests (OGTTs). A standard OGTT with 75 g glucose (Tru-Glu100, Fisher Scientific, Pittsburgh, PA) was conducted after 12 h of overnight fasting on the first day of admission. An iv catheter was placed in a forearm vein, and blood was collected for determination of glucose and insulin concentrations before glucose administration and at 30-min intervals thereafter for 180 min.
Anthropometric measurements. Height and weight were measured by standard procedures. Waist and hip circumferences were measured, using a flexible measuring tape with a tension caliper at the extremity (Gulick-Creative Health Product, Inc., Plymouth, MI), midway between the xiphoid and the umbilicus during the midinspiratory phase and at the maximum circumference in the hip area, respectively. The waist to hip circumference (W/H) ratio was calculated for each subject. Skinfold thickness was measured at nine different anatomical sites [subscapular (diagonal and vertical), chest, midaxillary, abdominal (horizontal and vertical), suprailiac (diagonal and vertical), triceps, biceps, thigh, and calf], using a Lange skinfold caliper (Cambridge Scientific Industries, Inc., Cambridge, MD). The same investigator (M.C.) performed all skinfold measurements to minimize interinvestigator variability. The means of three repeat measurements at each site were used for calculations. The horizontal/diagonal and vertical measurements of the subscapular, suprailiac, and abdominal skinfolds were averaged. The sum of truncal skinfold thickness was calculated by adding the skinfold thickness of subscapular, midaxillary, chest, abdomen, and suprailiac sites, and the sum of peripheral skinfold thickness was calculated by adding skinfold thickness of triceps, biceps, thigh, and calf regions. Body composition was studied by determination of body density in a Whitmore volumeter (Whitmore Enterprises, San Antonio, TX). Each subject was submerged in water up to the chin in a seated position. Then he was given 3000 mL gas to rebreathe (45% oxygen, 10% helium, and 45% nitrogen) and went completely underwater. Total volume displacement was measured to the nearest 50 mL. After resurfacing, the helium (He) concentration was measured in the exhaled gas by mass spectrometry (model 1100, Perkin Elmer, St. Louis, MO). Total submerged gas volume was calculated by the formula: total gas volume (mL) = 300 mL He/final He conc. + 100 mL (for abdominal gas). Total gas volume was subtracted from total displacement volume to give total body volume. Total body mass (kilograms), measured to the nearest 0.1 kg, was divided by body volume to obtain body density. Siri’s equation (30) was used to estimate the percentage of total body fat, lean body mass, and total fat mass.
Euglycemic, hyperinsulinemic clamp study. Clamp studies were conducted on the last day of admission after an overnight fast. A primed continuous infusion of regular insulin (Humulin, Squibb-Novo, Princeton, NJ) was given iv at a rate of 20 mU/m2·min from 0–120 min. Blood samples were obtained every 5 min from a catheter placed retrograde in a dorsal vein of a hand kept in a radiant warmer at 70 C to arterialize venous blood. Dextrose solution (20%) was infused iv to maintain plasma glucose at the fasting levels throughout the clamp procedure, according to the method of DeFronzo et al. (31). To study glucose turnover, a primed continuous iv infusion of [3-3H]glucose (DuPont-NEN, Boston, MA) was started at a rate of 2.36 nCi/kg·min at 120 min before the initiation of insulin infusion (-120 min) and was continued throughout the duration of the clamp. To minimize the physiologically unacceptable negative values of hepatic glucose output (HGO) during the hyperinsulinemic phase of the study, the 20% dextrose solution was "spiked" with [3-3H]glucose to maintain a constant specific activity according to the method of Finegood et al. (32). Blood samples for measurement of glucose, insulin, and [3-3H]glucose specific activity were collected at 10-min intervals from -40 to 0 min before and from 80–120 during the study. The rate of glucose appearance (Ra) in plasma was calculated by measuring specific activity of [3-3H]glucose in the plasma using the one-compartment model described by Steele et al. (33) and modified, for labeled variable glucose infusion, by Finegood et al. (32), assuming a volume of distribution of 210 mL/kg. Endogenous glucose production or HGO during the clamp was calculated as the difference between the Ra and the glucose infusion rate for the time interval, and negative values, if any, were assumed to be equal to zero. The rate of glucose disposal (Rd) was calculated by subtracting the urinary glucose excretion from the Ra and using space correction. The data for HGO and Rd are presented in milligrams per min/kg lean body mass.
Biochemical analyses. Plasma and urinary glucose concentrations were assayed using a glucose oxidase method (glucose analyzer, Beckman Coulter, Inc., Fullerton, CA). The specific activity of glucose was determined from the plasma samples deproteinized by barium hydroxide and zinc sulfate precipitation, according to the method of Meneilly et al. (34). Plasma insulin levels were determined by a modification (35) of the RIA described by Yalow and Berson (36).
Statistical analysis
Statistical analysis was performed using BMDP (SPSS, Inc., Chicago, IL). Due to the skewness of some data (e.g. triglycerides), the nonparametric Mann-Whitney U test was used to compare the Caucasians and Asian Indians. Regression analysis was used to assess the relationship between Rd values and regional adiposity and to compare the regression lines between the two groups. Due to the curvilinear trend, the regression analysis was also performed using the log-transformed dependent variable. As the transformed results were essentially the same as the original units, the untransformed results are reported.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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, the general
characteristics of Asian Indian subjects are compared with those of the
Caucasian subjects. Despite the similar age range, the mean age of
Caucasian subjects was slightly higher than that of the Asian Indian
subjects. The average body mass indexes for the two groups were
similar. Fasting plasma glucose, total cholesterol, total
triglycerides, and low density lipoprotein cholesterol were similar in
both the groups. However, plasma high density lipoprotein (HDL)
cholesterol concentrations were significantly lower in the Asian Indian
group.
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. Mean plasma
glucose and insulin levels were higher in the Asian Indian group at all
time points during the OGTT. The areas under the curve for both plasma
glucose and insulin were significantly higher in the Asian Indian group
(P = 0.02 and P = 0.004 for glucose and
insulin, respectively). The data for body composition and fat
distribution are summarized in Table 2.
There was no difference in the percentage of total body fat mass
between the two groups. Both waist and hip circumferences were lower in
Asian Indians compared to Caucasians, although the difference did not
reach statistical significance. However, the sums of truncal skinfold
thickness were significantly higher in Asian Indians compared to
Caucasians, whereas the sums of peripheral skinfold thickness were
similar between the groups (see also Fig. 2). Truncal to peripheral skinfold ratios
were significantly higher in Asian Indians, but waist to hip ratios
were similar in both groups. In Fig. 3, the individual data on skinfold thickness in various anatomical sites
in the two study groups are compared. Overall, the skinfold thickness
of all truncal areas was higher in the Asian Indian group, although a
statistically significant difference was observed only for the chest
and subscapular areas. The sum of the skinfold thickness in all
peripheral areas was similar for both groups.
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is a summary of the results of
the euglycemic-hyperinsulinemic clamp studies. Plasma insulin levels
during fasting and infusion were significantly higher in Asian Indians
compared to Caucasians. Fasting HGO were similar in both groups and
were suppressed to a similar extent in both groups during the
hyperinsulinemic clamp. The rate of glucose disposal was significantly
lower in Asian Indians than that in Caucasians.
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and 5
illustrate the relationships between total body fat and truncal
skinfold thickness and the insulin sensitivity index. The regression
curves shown in Figs. 4 and 5 illustrate that for any given amount of
adipose tissue in either the total body or truncal area, the Asian
Indians had lower insulin sensitivity to insulin-mediated glucose
disposal. This apparent difference was further examined by comparing
the regression lines between the insulin sensitivity index and truncal
adipose tissue for the two groups. The slopes of the regression lines
for total body fat were similar for the two groups (P =
0.09). However, the intercept of insulin sensitivity index for the
regression line was significantly lower for Asian Indian subjects than
for Caucasian subjects (P = 0.002). Similarly, the
slopes of the regression lines for the sum of truncal skinfold
thickness were similar for the two groups (P = 0.14),
but the intercept was significantly lower for the Asian Indians than
for the Caucasian subjects (P = 0.04). A subgroup
analysis including the subjects with total body fat less than 20% of
total body mass confirmed that the insulin sensitivity index was
significantly lower in the Asian Indians compared to the Caucasians
(6.23 ± 1.63 and 4.17 ± 1.46 mg/min·kg lean body mass,
respectively; P = 0.009). The insulin sensitivity index
in the Asian Indians remained significantly lower than that in the
Caucasians after adjustment for both total body fat and truncal
skinfold thickness (P = 0.04).
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Discussion |
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One hypothesis has been proposed that could account for the high frequency of both type 2 diabetes and premature CHD in Asian Indians. This hypothesis maintains that Asian Indians are susceptible to a generalized metabolic condition commonly called the insulin resistance syndrome (1). Prolonged insulin resistance confers an increased risk for the development of type 2 diabetes (37), which is an independent risk factor for CHD. In addition, insulin resistance is often accompanied by other coronary risk factors, e.g. dyslipidemia and hypertension (38, 39, 40). Finally, it is possible that insulin resistance affects CHD risk status through other mechanisms that are independent of the established risk factors.
Several lines of evidence suggest that Asian Indians are predisposed to developing insulin resistance, based on the usual features of this syndrome. These include a relatively high prevalence of type 2 diabetes (1, 2, 3, 4, 5, 6, 7), a tendency to truncal obesity (12, 14, 20), an increased frequency of fasting hyperinsulinemia (13, 16), and other metabolic indicators of insulin resistance; among the latter are a hyperinsulinemic response to an oral glucose challenge (13, 16) and abnormal steady state concentrations of glucose during an insulin suppression test with somatostatin (17). The present study was carried out to determine whether a propensity to insulin resistance could be confirmed by glucose clamp studies. The glucose clamp technique provides quantitative data for one parameter of insulin sensitivity, namely rates of glucose disposal at a given level of plasma insulin.
The current study compared young adult Asian Indian men living in the United States with Caucasian American men. The subjects were of comparable age and body fat content. As previously reported (13, 14, 15, 16, 17), the Asian Indian men in this study had significantly higher fasting levels of insulin than Caucasian men did; however, differences were not as marked as has been reported previously. More striking differences were noted for the area under the curve of plasma insulin response to an oral glucose challenge. These differences strongly suggest that Asian Indian men as a group are insulin resistant compared to matched Caucasian men. This tendency was confirmed with euglycemic-hyperinsulinemic glucose clamp studies. Average rates of glucose disposal were markedly reduced in Asian Indians compared to those in Caucasians. A significant decrease in insulin sensitivity apparently was present in Asian Indian men regardless of the level of total body fat. This finding raises the possibility that the insulin resistance in Asian Indians can occur independently of an increase in total body fat content. However, when the glucose sensitivity index was plotted against the percent total body fat, an increasing percentage of body fat was accompanied by decreasing insulin sensitivity. Thus, it appears that whereas relatively lean Asian Indian men may be more insulin resistant than Caucasians of similar body fat content, increasing obesity is still accompanied by a decrease in insulin sensitivity.
An association between insulin sensitivity and body fat distribution has been observed in many studies (24, 25, 26, 27, 28, 29, 40, 41, 42, 43). Patients who have high waist to hip ratios usually are more resistant to the action of insulin than those with low ratios. Some investigators contend that ip (visceral) fat is the compartment of adipose tissue most tightly linked with insulin resistance (26, 27, 28). Recent studies from our laboratory (41, 42) and others (43), however, indicate that sc fat in the trunk is even better correlated with insulin sensitivity than is ip fat. This is true in both nondiabetic subjects and those with type 2 diabetes. The mechanism underlying this association is not known, although Jensen et al. (44) showed that patients with upper body obesity (truncal obesity) have higher levels of nonesterified fatty acids (NEFA) than do those with lower body obesity (gluterofemoral obesity). These high NEFA levels could lead to an increased fatty acid content of muscle and to inhibition of glucose oxidation (45). Possibly truncal adipose tissue more readily releases NEFA into the circulation than does gluterofemoral adipose tissue (46, 47).
Several reports indicate that Asian Indians are predisposed to upper body obesity. This tendency is reflected in reports of increased waist to hip ratios and increased truncal skinfold thicknesses in Asian Indians compared to other populations (10, 17, 20). The propensity to upper body obesity was confirmed in the present study. Compared to Caucasian men, Asian Indian men in this study had significantly thicker truncal skinfolds. In addition, the Asian Indians had higher ratios of truncal to peripheral skinfold thickness. It is interesting that in this group the thickness of skinfolds was a better indicator of predominant truncal fat accumulation than was the waist to hip ratio and the waist circumference. The lack of difference in waist circumference between Asian Indians and Caucasians suggests that a greater difference existed between sc truncal fat than between ip fat; however, definite proof of the latter would require studies that image ip fat. As other workers have reported that waist circumference tends to be greater in some groups of Asian Indians (14, 20), it is possible that more upper body obesity exists in all of the adipose tissue compartments of Asian Indians. As we previously observed in Caucasians, the sum of the truncal skinfolds was highly (and inversely) correlated with insulin sensitivity.
One of the most interesting observations of the current study was a strong tendency for insulin resistance in lean Asian Indians. The latter were much more insulin resistance than lean Caucasians. Although the curve of insulin sensitivity against percent body fat was relatively steep in Caucasians, this was not the case in Asian Indians. Among the latter, increasing adiposity was accompanied by some reduction in insulin sensitivity, but decrements were relatively small. This finding thus strongly suggests that Asian Indian men living in the United States have relatively low insulin sensitivity even when their body fat content is in the normal range. The mechanisms responsible for the low insulin sensitivity in Asian Indians, whether due to physical inactivity, dietary differences, or hereditary factors, remain to be determined.
The current findings seemingly do not support the concept that upper body fat distribution is the primary cause of insulin resistance in Asian Indians. First, lean Asian Indians were more insulin resistant than lean Caucasians, indicating that Asian Indians are insulin resistant with little or no upper body obesity. Second, although Asian Indians as a group showed a significant trend toward more truncal fat than Caucasians, Asian Indians appeared to be more insulin resistant at any level of truncal skinfold thickness. Thus, truncal obesity (or predominant upper body fat) seemingly cannot be the primary cause of low insulin sensitivity in Asian Indians.
Current and previous data indicate that Asian Indians are predisposed to truncal obesity. Previous studies have shown that the degree of truncal obesity is inversely correlated with insulin sensitivity (41, 42). According to current concepts, truncal adipose tissue has a propensity to excessive release of NEFA, which may impair insulin sensitivity. Thus, the tendency of Asian Indians to develop truncal obesity could accentuate insulin resistance in a population that inherently has a low insulin sensitivity.
Alternatively, the propensity to truncal obesity in Asian Indians could be secondary to an underlying insulin resistance. Factors that determine the distribution of body fat are not known; the possibility that abnormal insulin action at the level of adipose tissue could promote the accumulation of truncal fat cannot be excluded.
As discussed before, other investigators have indicated that the established CHD risk factors can explain only a portion of the increased risk for CHD in Asian Indians living in urban settings. In the present study, the only established risk factor that was more prevalent in the Asian Indians was a lower level of HDL cholesterol. A low HDL cholesterol concentration has been noted previously to be strongly associated with insulin resistance (48, 49). The mechanism is not known, but may be related to an increase in hepatic lipase activity accompanying insulin resistance in the liver (50). However, a lower HDL cholesterol level and other major risk factors for CHD in Asian Indians cannot fully account for their increased risk for premature CHD. Instead, it appears that insulin resistance in Asian Indians is associated with causes of CHD that have yet to be elucidated. The current study confirms that Asian Indians are susceptible to insulin resistance. This condition is evoked by mild or even minimal increases in body fat content. Whereas it is true that Asian Indian men preferentially deposit body fat in the trunk, compared to Caucasians, our results suggest that predominant upper body fat is not a direct cause of the increased insulin resistance in Asian Indians.
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Acknowledgments |
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Footnotes |
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Received January 7, 1999.
Revised March 12, 1999.
Accepted March 19, 1999.
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References |
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