| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
From the Clinical Research Centers |
Department of Medicine, State University of New York Health Science Center, Brooklyn, New York 11203
Address all correspondence and requests for reprints to: Mary Ann Banerji, M.D., State University of New York Health Science Center, 450 Clarkson Avenue, Box 1205, Brooklyn, New York 11203. E-mail address: banerm05{at}hscbklyn.edu
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
A mean body mass index of 24.5 ± 2.5 kg/m2 was associated with an unusually high percentage of body fat (33 ± 7%). The majority of the fat was sc, and 16% was visceral (intraabdominal) adipose tissue. The majority (66%) of these nonobese men were insulin resistant. The mean fasting serum leptin level was 7.6 ± 3.3 ng/mL.
Insulin action was inversely correlated with visceral adipose tissue, not total or abdominal sc adipose tissue. In contrast, leptin levels correlated with sc and total (not visceral) adipose tissue. Serum triglyceride and high density lipoprotein cholesterol levels were inversely correlated with each other and were directly related to insulin resistance and visceral (not subcutaneous) fat.
Increased visceral fat in Asian Indians is associated with increased generalized obesity, which is not apparent from their nonobese body mass index. Increased visceral fat is related to dyslipidemia and increased frequency of insulin resistance and may account for the increased prevalence of diabetes mellitus and cardiovascular disease in Asian Indians.
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
24 kg/m2) do
not suggest generalized obesity (5, 9). Among Caucasians and
African-Americans, the BMI values of Asian Indians would not be
associated with such a high prevalence of insulin resistance.
Epidemiological studies suggest that the distribution of fat,
especially visceral obesity, may be a more important determinant of
insulin resistance, diabetes, and cardiovascular disease than
generalized obesity (19, 20, 21, 22). Data relating the increase in the
prevalence of type 2 diabetes in Asian Indians to the waist/hip ratio
(WHR) are controversial (5, 9), and detailed studies of body fat
distribution in relation to insulin resistance have not been reported.
This study was designed to test the hypothesis that insulin resistance
and dyslipidemia are related to visceral, not sc, adipose tissue volume
and to explore the role of plasma leptin in migrant Asian Indians
living in the United States. We measured peripheral insulin action using the euglycemic insulin clamp with a 6 nmol/kg/min insulin infusion and correlated this with measures of body composition obtained from 22-slice computed tomography (CT), including total adipose tissue volume, total sc adipose tissue volume, total regional adipose tissue volumes, and total muscle volume. We correlated these measures with fasting serum lipid and leptin levels.
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Twenty Asian Indian healthy male volunteers without a known
history of diabetes were studied (mean ± SD age,
38.6 ± 10 yr; BMI, 24.5 ± 2.5 kg/m2; Table 1
). The subjects were professionals
working at the medical center. Oral glucose tolerance testing (2 h with
75 g oral glucose) showed a mean ± SD fasting
plasma glucose of 5.6 ± 0.55 and 2-h plasma glucose of 6.88
± 2.0 mmol/L. Ten of 20 subjects had a first degree family history of
diabetes mellitus. Four subjects had impaired glucose tolerance based
on the WHO (23) criteria (mean fasting plasma glucose, 5.66 ±
0.28; 2-h plasma glucose, 9.44 ± 0.89 mmol/L). One subject was
diabetic (BMI, 23.5; hemoglobin A1C, 6.2%; fasting plasma
glucose, 7.6 mmol/L; 2-h plasma glucose, 12.1 mmol/L). Subjects had
maintained a constant body weight for at least 3–4 months before the
study. None had significant renal, hepatic, or cardiac disease, and
none was using agents known to affect glucose metabolism. The control
population for plasma insulin during the oral glucose tolerance test
consisted of 15 normal African-American men with a similar mean age of
38.9 ± 12 yr and BMI of 25.59 ± 1.5 kg/m2. All
subjects were instructed to consume at least 150 g carbohydrate
for 3 days before any study and had fasted overnight before morning
studies.
|
Body composition determined by computed axial tomography
A GE Pace scanner (Milwaukee, WI) was used to calculate the total intraabdominal (visceral) and total and abdominal sc adipose tissue volume and total muscle volume. Scanning was performed at 120 kV with a slice thickness of 5 mm, with the subjects’ arms stretched over their heads. Twenty-two scans were performed at the anatomical levels recommended by Sjöström (24). Techniques for analysis and volume calculations have been previously described (21).
Anthropometric measurements
Using a tape measure, with the subject standing, the waist was measured as the narrowest circumference between the lower costal margin and the iliac crest. The hip was the maximum circumference at the level of the femoral trochanters.
Insulin sensitivity
Insulin sensitivity was measured using the euglycemic hyperinsulinemic clamp with a 6 nmol/kg/min insulin infusion, as previously described (21). At this level of insulin infusion, hepatic glucose production is virtually negligible in diabetic and nondiabetic subjects (25, 26, 27). Plasma glucose was clamped at fasting euglycemic levels (coefficient of variance of 5%). Glucose disposal was measured during the last hour of the 2-h insulin infusion when the plasma insulin level was 540 ± 12 pmol/L (mean ± SEM). Insulin resistance was defined as a glucose disposal rate of less than 30 µmol/kg/min, which is 2 SD below the mean of nondiabetic African American control subjects (27) and not different from those of numerous control populations reported in the literature (28).
Analytical method
Plasma glucose was measured by a glucose oxidase method using a Beckman Coulter, Inc. glucose analyzer (Fullerton, CA). Plasma insulin was measured with a double antibody RIA technique with a lower limit of detection of 15 pmol/L, using a kit purchased from Incstar Corp. (Stillwater, MN). Hemoglobin A1c was determined using the Bayer DCA 2000 (West Haven, CT), with an upper limit of normal of 6.3%. Serum leptin was measured using a double antibody RIA kit from Linco Research, Inc. (St. Charles, MO), with a lower limit of detection of 0.5 ng/mL.
Materials
Human insulin was supplied by Eli Lilly & Co. (Indianapolis, IN).
Statistical analysis
Group means were compared using Student’s t test. Linear and multiple regression and Ridge regression analyses were performed (29). Data are expressed as the mean ± SD.
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
and 2. Despite a mean body mass
index of 24.5 kg/m2, the subjects had significantly
elevated mean fasting and 2-h postoral glucose load plasma insulin
levels compared to nondiabetic African American men using the same
insulin assay (BMI, 25.5 ± 1.5 kg/m2; fasting and 2
hour plasma insulin levels, 60 ± 24 and 354 ± 180 pmol/L;
P < 0.02 and 0.05). These are similar to reports of
hyperinsulinemia in Asian Indians compared with different ethnic groups
(13, 16). This occurred even though the mean fasting and 2-h postoral
glucose plasma glucose levels were within the normal range based on WHO
criteria (fasting and 2-h plasma glucose, <7.8 and <11.1 mmol/L,
respectively) (23). The mean waist circumference (86.2 cm) and WHR
(0.88) were less than the established normal ranges for other
populations (30).
|
Direct assessment of insulin action or insulin-mediated glucose
disposal measured during a physiological infusion of insulin (6
nm/kg/min) showed a mean ± SD of 25.0 ± 7.8
µmol/kg/min, ranging from 11.9–39.1 µmol/kg/min (Table 2). Two
thirds of the subjects (13 of 20) were insulin resistant, whereas only
one third (7 of 20) were normally insulin sensitive compared to our
published controls (27). Because glucose disposal is primarily a
function of muscle mass (31), we have also expressed it as glucose
disposal per kg lean body mass (LBM), which ranged from 22.3–64.7
µmol/kg-LBM/min. This expression of glucose disposal is used in all
subsequent analyses.
Body composition
Although the degree of insulin resistance in these subjects
appeared inconsistent with their normal BMI of 24.5 kg/m2,
CT measurement of body composition showed that their total body fat was
33 ± 7% (total adipose tissue divided by total body volume;
Table 3). By this criteria they are
significantly obese. This corresponded to a total body adipose tissue
volume of 20.75 ± 6.9 L. Eighty-one percent of the fat was sc
(16.9 ± 5.8 L), and 16.8%, or 3.48 ± 1.52 L, was located
in the intraabdominal or visceral compartment. The total visceral
adipose tissue volume correlated significantly with the other adipose
tissue depots: total body, total sc, and abdominal sc adipose tissue
volume (r = 0.73, P = 0.0001; r = 0.58,
P = 0.007; and r = 0.68, P =
0.001, respectively), and with BMI (r = 0.50, P =
0.025). Total muscle volume was 27.5 ± 3.6 L and represented
45 ± 6% of the body volume. The ratio of total fat/muscle was
0.75.
|
We next determined the extent to which insulin action was
correlated with generalized or regional adiposity. Table 4 shows that insulin-mediated glucose
disposal was significantly inversely correlated with all compartments
of adipose tissue, including total visceral adipose tissue volume,
abdominal sc adipose tissue volume, and total sc and total body adipose
tissue volume (r = -0.59, P = 0.006; r =
-0.54, P = 0.014; r = -0.49, P =
0.028; and r = -0.56, P = 0.014, respectively).
To determine which adipose tissue compartment was the more significant
predictor of insulin-mediated glucose disposal, we performed an overall
multivariate analysis that tested total body, visceral, and abdominal
sc adipose tissue volume entered in a stepwise fashion. Only visceral
adipose tissue volume was significantly (P < 0.005)
related to insulin-mediated glucose disposal and explained 38% of the
variance (Fig. 1). The nonsignificant
(both P > 0.32) terms (total and abdominal sc adipose
tissue volume) explained an additional 3% of the variance.
Additionally, a Ridge regression, performed to correct for the
multicolinearity of the independent variables, showed that visceral
adipose tissue was the significant predictor of glucose disposal
(P = 0.049), whereas abdominal sc adipose tissue was
not (P = 0.149). That is, after controlling for
abdominal sc adipose tissue volume, visceral adipose tissue volume was
still significantly (P = 0.049) related to
insulin-mediated glucose disposal. Multivariate analysis using the
absolute volumes adjusted for body surface area showed identical
results [visceral adipose tissue volume/m2 explained 32%
of the variance of glucose disposal (P < 0.0176);
abdominal sc and total adipose tissue volume were nonsignificant
(P > 0.35) and explained an additional 4% of the
variance). An analysis of the data excluding the single diabetic
subject (visceral adipose tissue volume, 6.13 L; glucose disposal, 28.9
µmol/kg-LBM/min) gave similar results: visceral adipose tissue volume
accounted for 31% (P = 0.001) of the variance in
glucose disposal, and abdominal sc and total adipose tissue volumes
were not significant (P > 0.39).
|
|
Anthropometry
Anthropometric measurements showed that the waist circumference
and the WHR were inversely correlated with insulin-mediated glucose
disposal (r = -0.63, P < 0.003 and r =
-0.48, P < 0.03, respectively; Table 4). Multiple
regression analysis with waist circumference and WHR entered stepwise
showed that the waist circumference explained 39% (P
< 0.003) of the variance in glucose disposal, whereas WHR was not a
significant (P = 0.791) predictor. The waist and the
WHR were also correlated with the total visceral adipose tissue volume
(r = 0.82 and r = 0.77; both P < 0.0001).
Multiple regression analysis with waist circumference and WHR entered
stepwise showed that waist circumference explained 67% of the variance
in visceral adipose tissue volume (P < 0.0001),
whereas the WHR explained a nonsignificant (P = 0.163)
additional 5%. Thus, the waist circumference is a better surrogate
than WHR for both visceral adipose tissue volume and insulin-mediated
glucose disposal.
The waist circumference, but not the WHR, was also correlated with abdominal sc adipose tissue volume (r = 0.82, P < 0.0001 and r = 0.41, P = 0.071). Despite its significant correlations, the waist circumference does not distinguish which of its two adipose tissue components (visceral or sc) is the more important predictor of insulin-mediated glucose disposal.
Lipids
Because of the high prevalence of coronary artery disease among
Asian Indians, we investigated the interrelationships of plasma lipids,
visceral adipose tissue, and insulin action (Table 5). The fasting serum triglyceride level
was 2.0 ± 1.15 mmol/L and was inversely related to serum high
density lipoprotein (HDL) cholesterol levels (1.01 ± 0.31 mmol/L;
r = -0.58, P = 0.007). Serum triglyceride levels
were inversely related to glucose disposal and positively correlated to
visceral adipose tissue volume (r = -0.45 and r = 0.46,
respectively; both P < 0.05). Multivariate analysis
with glucose disposal and visceral adipose tissue volume entered
stepwise showed that visceral adipose tissue volume significantly
(P < 0.04) explained 21% of the variance in fasting
serum triglyceride levels, whereas glucose disposal was not significant
(P = 0.34). HDL cholesterol was significantly
correlated with glucose disposal (r = 0.52, P <
0.018), but not with visceral adipose tissue volume (r = -0.38,
P = NS). The low density lipoprotein (LDL) cholesterol
level showed a trend toward a significant correlation with glucose
disposal (r = -0.42, P = 0.064). In contrast,
neither total sc nor abdominal sc adipose tissue was related to serum
lipid levels.
|
Although Asian Indians have increased generalized
adiposity, the metabolic abnormalities of insulin resistance and
dyslipidemia are related to visceral, not total or sc, adipose tissue.
Therefore, an obvious question was to which adipose tissue compartment
was leptin, a neuroregulatory hormone produced by fat cells, related.
Fasting serum leptin levels ranged from 3.3–16.8 ng/mL (mean, 7.6
ng/dL; Table 2). In contrast to glucose disposal, fasting serum leptin
levels were highly correlated with sc, but not visceral, adipose tissue
(r = 0.89, P < 0.0001 and r = 0.37;
P = NS; Fig. 2). As might
be expected, serum leptin was not correlated with glucose disposal or
plasma lipids. The correlation of leptin levels with BMI (r =
0.81, P < 0.0001) reflects the high correlation of BMI
to sc fat volume.
|
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
The data support the hypothesis that among Asian Indians, increased visceral, not sc, adipose tissue volume is associated with insulin resistance, hyperinsulinemia, and dyslipidemia and may explain their propensity for increased cardiovascular disease and diabetes. Plasma leptin levels, in contrast, are associated with sc adipose tissue volume.
Body composition
The increased insulin resistance requires an explanation because
the mean BMI (24 kg/m2) is considered neither obese nor
predisposing to diabetes in other populations, and controversy exists
as to whether insulin resistance is related to general or regional
adiposity in Asian Indians (5, 9, 32). A 5-fold increase in the
prevalence of diabetes is associated with an increase in BMI but no
change in the WHR in urban compared to rural Asian Indians in India
(5). In contrast, the 4-fold increase in diabetes is associated with a
lower or similar BMI and higher WHR in migrant Asian Indians in the
United Kingdom compared to Europeans (9). At every level of WHR, these
Asian Indians have higher plasma insulin levels and are more insulin
resistant than their European counterparts (9, 33). An insulin
suppression test suggested that Asian Indians were 60% more insulin
resistant than BMI-matched Caucasians living in the U.S. (34).
Our direct CT measures of body composition may help explain these
discrepancies. Asian Indian men have lower muscle mass and 30% more
total body fat than the African American diabetic men studied (using
identical CT methods) or whites, whether expressed in terms of total
body volume, total muscle volume, or BMI (Fig. 3 and Table 6) (30, 35). The high body fat and low
muscle mass may explain the high prevalence of hyperinsulinemia and the
greater risk for development of type 2 diabetes.
|
|
The distribution of adipose tissue appears not to be markedly different in Asian Indian compared to African-American diabetic men or Swedish men when using comparable CT methods. Visceral/total fat is 16.8% and 18.3% in Asian Indian and African American diabetic men (21) and 19% and 18.4% in Asian Indian and Swedish men, respectively (36). In contrast, anthropometry (BMI and WHR) suggested that migrant Asian Indians compared to Europeans have lower overall obesity, with a selective increase in central obesity (9).
Insulin resistance and regional adiposity
Our data from Asian Indian men and African American diabetic men
and women (21) indicate that ,visceral not abdominal, sc adipose tissue
mass is the principal adipose tissue determinant of insulin-mediated
glucose disposal. Most studies are consistent with these data. The
increase in total body fat in Asian Indians results in an increase in
visceral fat and an expected increase in insulin resistance. Plasma
insulin responses to oral glucose (a surrogate for insulin action) were
correlated with visceral adipose tissue (CT) (39, 40, 41). Glucose disposal
(clamp method) was inversely correlated with waist circumference in men
and women (42), and plasma insulin levels inversely were correlated
with the WHR in obese, but not lean, Asian Indians (43). Glucose
disposal was inversely correlated with visceral adipose tissue area
(CT) in obese (BMI, 35 kg/m2) and with total body fat in
lean (BMI, 25) nondiabetic premenopausal women (44). In contrast,
some report a greater correlation of insulin-mediated glucose disposal
with abdominal sc rather than visceral adipose tissue (45, 46, 47) in
subjects studied over a wide range of BMI (19–47
kg/m2). The reasons for these differences are unclear, but
may be related to race, degree of obesity, or the close correlation of
different adipose tissue compartments.
The importance of visceral fat can also be shown in intervention and longitudinal studies. Weight loss by diet or dexfenfluramine treatment showed improvement of insulin action and plasma insulin to be due to the loss of visceral, not abdominal sc, adipose tissue (48, 49, 50). Visceral fat and WHR are linked to the development of glucose intolerance in many populations, including Asian Indians (5, 9, 10, 19, 20, 51, 52, 53, 54).
Leptin
There are conflicting reports as to whether plasma leptin, the neuroregulatory peptide produced by fat cells, is associated with total body, sc or visceral adipose tissue (55, 56, 57). Most report a strong association of plasma leptin and leptin messenger RNA with BMI or percent body fat (55, 56) but do not report body fat distribution. In normoglycemic Asian Indian men, leptin was associated with the total (not visceral or sc) fat area in the abdominal region (single slice CT) (57). However, a Swedish study in twins using single slice magnetic resonance imaging reported visceral, not sc, adipose tissue to be the significant correlate of leptin levels (58). Our data clearly show that in Asian Indian men, plasma leptin is associated with sc, not visceral, adipose tissue volume or insulin-mediated glucose disposal.
|
Acknowledgments |
|---|
|
Footnotes |
|---|
Received March 10, 1998.
Revised August 27, 1998.
Revised September 1, 1998.
Accepted September 17, 1998.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
This article has been cited by other articles:
 |
|
 |
|
  P. Balagopal, N. Kamalamma, T. G. Patel, and R. Misra A Community-Based Diabetes Prevention and Management Education Program in a Rural Village in India Diabetes Care, June 1, 2008; 31(6): 1097 - 1104. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. W. Yeckel, J. Dziura, and L. DiPietro Abdominal Obesity in Older Women: Potential Role for Disrupted Fatty Acid Reesterification in Insulin Resistance J. Clin. Endocrinol. Metab., April 1, 2008; 93(4): 1285 - 1291. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-H. Hwang, D. T. Stein, N. Barzilai, M.-H. Cui, J. Tonelli, P. Kishore, and M. Hawkins Increased intrahepatic triglyceride is associated with peripheral insulin resistance: in vivo MR imaging and spectroscopy studies Am J Physiol Endocrinol Metab, December 1, 2007; 293(6): E1663 - E1669. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. J Shaw, N. J Crabtree, M. S Kibirige, and J. N Fordham Ethnic and gender differences in body fat in British schoolchildren as measured by DXA Arch. Dis. Child., October 1, 2007; 92(10): 872 - 875. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. E Ruhl, T. B Harris, J. Ding, B. H Goodpaster, A. M Kanaya, S. B Kritchevsky, E. M Simonsick, F. A Tylavsky, J. E Everhart, and for the Health ABC Study Body mass index and serum leptin concentration independently estimate percentage body fat in older adults Am. J. Clinical Nutrition, April 1, 2007; 85(4): 1121 - 1126. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Kralisch, M. Bluher, A. Tonjes, U. Lossner, R. Paschke, M. Stumvoll, and M. Fasshauer Tissue inhibitor of metalloproteinase-1 predicts adiposity in humans Eur. J. Endocrinol., February 1, 2007; 156(2): 257 - 261. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Koutsari and M. D. Jensen Thematic review series: Patient-Oriented Research. Free fatty acid metabolism in human obesity J. Lipid Res., August 1, 2006; 47(8): 1643 - 1650. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Retnakaran, A. J.G. Hanley, and B. Zinman Does Hypoadiponectinemia Explain the Increased Risk of Diabetes and Cardiovascular Disease in South Asians? Diabetes Care, August 1, 2006; 29(8): 1950 - 1954. [Full Text] [PDF]
|
|
|
|
 |
|
 M. Gupta, N. Singh, and S. Verma South Asians and Cardiovascular Risk: What Clinicians Should Know Circulation, June 27, 2006; 113(25): e924 - e929. [Full Text] [PDF]
|
|
|
|
|
|
G. M Reaven The metabolic syndrome: is this diagnosis necessary? Am. J. Clinical Nutrition, June 1, 2006; 83(6): 1237 - 1247. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-P. Despres Abdominal obesity: the most prevalent cause of the metabolic syndrome and related cardiometabolic risk Eur. Heart J. Suppl., May 1, 2006; 8(suppl_B): B4 - B12. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Retnakaran, A. J. G. Hanley, P. W. Connelly, M. Sermer, and B. Zinman Ethnicity Modifies the Effect of Obesity on Insulin Resistance in Pregnancy: A Comparison of Asian, South Asian, and Caucasian Women J. Clin. Endocrinol. Metab., January 1, 2006; 91(1): 93 - 97. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. A Kensara, S. A Wootton, D. I Phillips, M. Patel, A. A Jackson, M. Elia, and Hertfordshire Study Group Fetal programming of body composition: relation between birth weight and body composition measured with dual-energy X-ray absorptiometry and anthropometric methods in older Englishmen Am. J. Clinical Nutrition, November 1, 2005; 82(5): 980 - 987. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. E. Lebovitz and M. A. Banerji Point: Visceral Adiposity Is Causally Related to Insulin Resistance Diabetes Care, September 1, 2005; 28(9): 2322 - 2325. [Full Text] [PDF]
|
|
|
|
|
|
H. S Sachdev, C. H. Fall, C. Osmond, R. Lakshmy, S. K Dey Biswas, S. D Leary, K. S. Reddy, D. J. Barker, and S. K Bhargava Anthropometric indicators of body composition in young adults: relation to size at birth and serial measurements of body mass index in childhood in the New Delhi birth cohort Am. J. Clinical Nutrition, August 1, 2005; 82(2): 456 - 466. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N P Grandhe, A Bhansali, S Dogra, and B Kumar Acanthosis nigricans: relation with type 2 diabetes mellitus, anthropometric variables, and body mass in Indians Postgrad. Med. J., August 1, 2005; 81(958): 541 - 544. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Ehtisham, N. Crabtree, P. Clark, N. Shaw, and T. Barrett Ethnic Differences in Insulin Resistance and Body Composition in United Kingdom Adolescents J. Clin. Endocrinol. Metab., July 1, 2005; 90(7): 3963 - 3969. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Dandona, A. Aljada, A. Chaudhuri, P. Mohanty, and R. Garg Metabolic Syndrome: A Comprehensive Perspective Based on Interactions Between Obesity, Diabetes, and Inflammation Circulation, March 22, 2005; 111(11): 1448 - 1454. [Full Text] [PDF]
|
|
|
|
 |
|
 S. E. Stern, K. Williams, E. Ferrannini, R. A. DeFronzo, C. Bogardus, and M. P. Stern Identification of Individuals With Insulin Resistance Using Routine Clinical Measurements Diabetes, February 1, 2005; 54(2): 333 - 339. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. L. Kind, C. T. Roberts, A. I. Sohlstrom, A. Katsman, P. M. Clifton, J. S. Robinson, and J. A. Owens Chronic maternal feed restriction impairs growth but increases adiposity of the fetal guinea pig Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2005; 288(1): R119 - R126. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Garg Regional Adiposity and Insulin Resistance J. Clin. Endocrinol. Metab., September 1, 2004; 89(9): 4206 - 4210. [Full Text] [PDF]
|
|
