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PubMed2002

Relationship between visceral fat accumulation and anti-lipolytic action of insulin in patients with type 2 diabetes mellitus.

Insulin resistance is closely related to developing type 2 diabetes mellitus. Visceral fat accumulation is associated with insulin resistance, which affects the free fatty acid (FFA) metabolism. We investigated the interactions among visceral fat accumulation, FFA metabolism and insulin resistance in 20 patients with type 2 diabetes mellitus, including 11 obese and 9 non-obese subjects. Body fat distribution was estimated by measuring the areas of both subcutaneous and visceral fat mass on abdominal computed tomography at the umbilical level. Glucose infusion rate (GIR) and plasma FFA responses to insulin were determined as an index of insulin resistance and anti-lipolytic action, respectively, in a euglycemic hyperinsulinemic clamp study. There was an inverse correlation between GIR and insulin-induced decrease in plasma FFA in all diabetic patients (r = -0.652, P < 0.01). Visceral fat mass area was well correlated with GIR (r = -0.583, P < 0.01) and insulin-induced decrease in plasma FFA (r = 0.724, P < 0.001), whereas subcutaneous fat mass area was not correlated either with GIR or plasma FFA decrease. These findings suggest that visceral fat accumulation results in increasing the resistance against the anti-lipolytic action of insulin, and that FFA metabolism is closely related with glucose utilization in patients with type 2 diabetes mellitus.

Adipose Tissue↗
PubMed2006

Do changes in body mass index percentile reflect changes in body composition in children? Data from the Fels Longitudinal Study.

OBJECTIVE: Our aim was to examine the degree to which changes in BMI percentile reflect changes in body fat and lean body mass during childhood and how age and gender affect these relationships. METHODS: This analysis used serial data on 494 white boys and girls who were aged 8 to 18 years and participating in the Fels Longitudinal Study (total 2319 observations). Total body fat (TBF), total body fat-free mass (FFM), and percentage of body fat (%BF) were determined by hydrodensitometry, and then BMI was partitioned into its fat and fat-free components: fat mass index (FMI) and FFM index (FFMI). We calculated predicted changes (Delta) in FMI, FFMI, and %BF for each 10-unit increase in BMI percentile using mixed-effects models. RESULTS: FFMI had a linear relationship with BMI percentile, whereas FMI and %BF tended to increase dramatically only at higher BMI percentiles. Gender and age had significant effects on the relationship between BMI percentile and FFMI, FMI, and %BF. Predicted Delta%BF for boys 13 to 18 years of age was negative, suggesting loss of relative fatness for each 10-unit increase in BMI percentile. CONCLUSIONS: In this longitudinal study of white children, FFMI consistently increased with BMI percentile, whereas FMI and %BF had more complicated relationships with BMI percentile depending on gender, age, and whether BMI percentile was high or low. Our results suggest that BMI percentile changes may not accurately reflect changes in adiposity in children over time, particularly among male adolescents and children of lower BMI.

Adolescent↗
PubMed2006

[Lipid profile and anthropometrical evaluation in type 1 diabetes].

Intensive insulin therapy in patients with type 1 diabetes is resulting in a better clinic and metabolic control. On the other hand, an increase in overweight and obesity prevalence, which could contribute to a higher risk of cardiovascular disease, has been observed. The aim of our study is to analyze the demographics, clinical and laboratorial factors associated to the presence of dyslipidemia in a group of patients with type 1 diabetes compared to a non-diabetic population. We have studied 72 type 1 diabetics: 52.8% female, aged 22.7 +/- 9.6 years old, with a body mass index (BMI) of 21.1 +/- 3.1 Kg/m2 and 66 non-diabetic patients: 60.6% female, aged 23.1 +/- 10.9 years old and a BMI of 22.12 +/- 3.7 Kg/m2. The group included 13 children (6 with type 1 diabetes), 47 adolescents (23 with type 1 diabetes) and 78 adults (43 with type 1 diabetes). We have found in the adult population with type 1 diabetes a lower overweight prevalence and lower levels of apoB (p< 0.01) and a higher apoA/apoB ratio (p< 0.01) when compared to the non-diabetic population. We have not found difference in the lipid profile in adult groups. Diabetic children and adolescents had higher frequency of total cholesterol (p= 0.02 and p< 0.01, respectively) and LDL-cholesterol (p= 0.02 and p= 0.01 respectively) above the upper limit when compared to the non-diabetic group. We concluded that the conventional methods for detecting lipids alterations in outpatients with type 1 diabetes under routine care are not sufficient to identify the lipid alterations, which could be related to the higher risk of cardiovascular disease in adult population.

Adolescent↗
PubMed2003

Insulin secretion, insulin sensitivity, and hepatic insulin extraction in first-degree relatives of type 2 diabetic patients.

To identify early metabolic abnormalities in type 2 diabetes mellitus, we measured insulin secretion, sensitivity to insulin, and hepatic insulin extraction in 48 healthy normal glucose-tolerant Brazilians, first-degree relatives of type 2 diabetic patients (FH+). Each individual was matched for sex, age, weight, and body fat distribution with a person without history of type 2 diabetes (FH-). Both groups were submitted to a hyperglycemic clamp procedure (180 mg/dl). Insulin release was evaluated in its two phases. The first was calculated as the sum of plasma insulin at 2.5, 5.0, 7.5, and 10.0 min after the beginning of glucose infusion, and the second as the mean plasma insulin level in the third hour of the clamp procedure. Insulin sensitivity index (ISI) was the mean glucose infusion rate in the third hour of the clamp experiment divided by the mean plasma insulin concentration during the same period of time. Hepatic insulin extraction was determined under fasting conditions and in the third hour of the clamp procedure as the ratio between C-peptide and plasma insulin levels. FH+ individuals did not differ from FH- individuals in terms of the following parameters [median (range)]: a) first-phase insulin secretion, 174 (116-221) vs 207 (108-277) microU/ml, b) second-phase insulin secretion, 64 (41-86) vs 53 (37-83) microU/ml, and c) ISI, 14.8 (9.0-20.8) vs 16.8 (9.0-27.0) mg kg-1 min-1/ microU ml-1. Hepatic insulin extraction in FH+ subjects was similar to that of FH- ones at basal conditions (median, 0.27 vs 0.27 ng/microU) and during glucose infusion (0.15 vs 0.15 ng/ micro U). Normal glucose-tolerant Brazilian FH+ individuals well-matched with FH- ones did not show defects of insulin secretion, insulin sensitivity, or hepatic insulin extraction as tested by hyperglycemic clamp procedures.

Adult↗
PubMedDate not supplied

Treatment with pergolide or cyproheptadine of pituitary pars intermedia dysfunction (equine Cushing's disease).

Medical records of 27 horses (including 13 ponies) treated with pergolide or cyproheptadine for pituitary pars intermedia dysfunction were reviewed to determine the effect of treatment on plasma ACTH, insulin, and glucose concentrations and clinical signs. Prior to treatment, the most common clinical signs were laminitis, hirsutism, and abnormal body fat distribution. The median pergolide dose was 3.0 microg/kg p.o. q24h (range, 1.7-5.5 microg/kg). All horses treated with cyproheptadine were given 0.25 mg/kg p.o. q24h. After pergolide treatment, ACTH concentrations (n = 20; median = 30.4 pg/ml; range, 4.2-173) were significantly lower (P < .01) than those in horses treated with cyproheptadine (n = 7; median = 141.0 pg/ml: range, 10-1,230). Among horses treated with pergolide, there was a correlation between ACTH concentration after treatment and the duration of treatment (P < .001) and pergolide dose (P = .04). Significantly (P = .02) more owners of horses treated with pergolide (85%, 17/20) reported an improvement in clinical signs compared to owners of horses treated with cyproheptadine (28%, 2/7).

Adrenocorticotropic Hormone↗
PubMed2006

Role of opioid antagonists in the treatment of women with glucoregulation abnormalities.

Beta-endorphin were detected in the endocrine pancreas and seem able to influence insulin and glucagon release. Hence, endogenous opioids could have a role in glucoregulation and in the pathogenesis of obesity beyond the previously detected effects on appetite. Metabolic abnormalities, such as hyperinsulinemia, insulin-resistance and obesity, are common features of polycystic ovary syndrome (PCOS), and seem to have a pathogenetic role in this disorder. A link between opioids and PCOS-related hyperinsulinism is suggested by the finding of altered central opioid tone and elevated beta-endorphins levels, directly correlated with body weight, in these patients. Furthermore, naloxone and naltrexone significantly reduce the insulin response to glucose load only in hyperinsulinemic PCOS patients. This effect is obtained chiefly through an improvement of insulin clearance. Naltrexone is also able to ameliorate the abnormal gonadotrophins secretion and to improve the ovarian responsiveness in obese PCOS women undergoing ovulation induction with exogenous GnRH. Such effects are believed to be obtained through an amelioration of hyperinsulinemia. Gonadal steroids modulate the opioid system both centrally and in peripheral districts. Nevertheless, the decline of ovarian function does not abolish the opioidergic control of glucoregulation. Post-menopausal period is characterised by a high prevalence of hyperinsulinemia and insulin-resistance. In particular, an association between hyperinsulinemia and increased opioid activity was found in postmenopausal women showing a central body fat distribution. Both naloxone and naltrexone ameliorate the metabolic imbalance also when it appears in the climacteric period, and mainly by increasing insulin clearance. The benefits of naltrexone may represent in the future a useful tool for the treatment of women with hyperinsulinism in the clinical practice.

Clinical Trials as Topic↗
PubMed1991

Insulin sensitivity in pregnancy.

Quantitation of insulin sensitivity (SI) with the insulin suppression test, glucose clamp, or the minimal model method has been achieved in various clinical circumstances. The application of these techniques to pregnancy has been limited. It is important to utilize sensitive and reproducible methods to study SI changes in pregnancy to fully understand the normal and pathological metabolic alterations that occur during gestation. These techniques demonstrate that various factors (obesity, body fat distribution, age, dietary manipulation, and exercise) may affect SI measures. The various pregnancy hormones have differential effects on insulin action. There is consensus among the limited in vivo studies in human pregnancy that late gestation is associated with significantly impaired SI compared with the nonpregnant state. Studies with appropriate matching between control and gestational diabetic subjects have failed to demonstrate a significant difference in SI between groups in the third trimester.

Diabetes, Gestational↗
PubMed1995

Higher proinsulin and specific insulin are both associated with a parental history of diabetes in nondiabetic Mexican-American subjects.

Both insulin resistance and decreased insulin secretion have been hypothesized to be precursors of non-insulin-dependent diabetes. An elevated proinsulin concentration reflects abnormal proinsulin processing and could indicate abnormal insulin secretion. We examined fasting insulin (measured by a radioimmunoassay that does not cross-react with proinsulin), as a marker of insulin resistance, and proinsulin and the fasting proinsulin-to-insulin ratio, as markers of impaired proinsulin processing, in 597 nondiabetic Mexican-Americans from the San Antonio Heart Study. Fasting insulin, proinsulin, and the fasting proinsulin-to-insulin ratio were higher in subjects with a parental history of diabetes than in subjects without such a history. These differences remained statistically significant after adjustment for obesity, body fat distribution, and glucose tolerance. A parental history of diabetes in nondiabetic Mexican-Americans is associated with an increase in fasting specific insulin and a disproportionate increase in proinsulin relative to insulin. These data suggest that both increased insulin resistance and abnormal processing of proinsulin are present in offspring of parents with diabetes.

Blood Glucose↗
PubMed1997

Insulin sensitivity and acute insulin response in African-Americans, non-Hispanic whites, and Hispanics with NIDDM: the Insulin Resistance Atherosclerosis Study.

NIDDM is usually characterized by beta-cell failure and decreased insulin sensitivity. It has been reported that a high proportion of African-American NIDDM subjects are insulin sensitive. To examine this issue, we determined insulin sensitivity (S(I)) in 479 NIDDM subjects by minimal model analyses of frequently sampled intravenous glucose tolerance (FSIGT) from the Insulin Resistance Atherosclerosis Study (IRAS), a large multicenter study of insulin sensitivity and cardiovascular risk in African-Americans, Hispanics, and non-Hispanic whites. The African-Americans and non-Hispanic whites were sampled in Los Angeles and Oakland, California. The non-Hispanic whites and Hispanics were sampled in San Antonio, Texas, and San Luis Valley, Colorado. We defined the proportion of insulin-sensitive (S(I)) subjects as > or =1.61 min-1 x microU-1 x ml-1, which is above the median for nondiabetic subjects of all ethnic groups in the IRAS. Using this definition, the proportion of insulin-sensitive diabetic subjects was very low in all ethnic groups (non-Hispanic whites [14.3%] vs. African-Americans [6.5%], P = 0.039 in Los Angeles and Oakland; non-Hispanic whites [6.8%] vs. Hispanics [4.9%], P = 0.737 in San Luis Valley and San Antonio). These results were also similar in newly diagnosed mildly hyperglycemic diabetic subjects. In addition, these results were not affected by the adjustment for differences in obesity, body fat distribution, and severity of hyperglycemia. Even in nonobese subjects (with BMI <30 kg/m2), the proportion of insulin-sensitive subjects (S(I) > or =1.61 min-1 x microU-1 x ml-1) was low (3.6-9.7%). The acute insulin response (AIR) was significantly higher in African-Americans than in non-Hispanic whites; there were no ethnic differences in AIR between Hispanics and non-Hispanic whites. There were no significant ethnic differences for non-insulin-mediated glucose disposal (S(G)). We conclude that the number of insulin-sensitive NIDDM subjects is low and similar among non-Hispanic whites, Hispanics, and African-Americans in the U.S.

Black or African American↗
PubMed1999

Obesity-related phenotypes and the beta3-adrenoceptor gene variant in postmenopausal women.

We examined the hypothesis that postmenopausal women with the beta3-adrenoceptor gene variant (Trp64Arg) have reduced total daily energy expenditure (TEE), altered free fatty acid kinetics, and increased intra-abdominal fat. A secondary objective was to examine whether the obese state masks the effect of the variant on resting metabolic rate (RMR). There were 23 obese heterozygous women with the genetic variant (age 58 +/- 6 years; BMI 36 +/- 7 kg/m2) who were compared with 19 homozygous obese women with the normal allele (age 56 +/- 4 years; BMI 36 +/- 3 kg/m2). Daily energy expenditure was determined from doubly labeled water and indirect calorimetry, lipolysis from infusion of [1-13C]palmitate, and body fat distribution from computed tomography. No significant differences were found in TEE, RMR, energy expenditure of physical activity, the thermic effect of a meal, fat oxidation as estimated by fasting and postprandial respiratory quotients (RQs), or rate of lipolysis. Similarly, no difference was found in visceral adipose tissue and abdominal subcutaneous fat areas. When RMR was compared between obese (n = 23) and never-obese women with the Trp64Arg variant (n = 16), we found a 317 kcal/day lower RMR in never-obese women after controlling for fat mass, fat-free mass, and age (P < 0.0017). These results do not support the hypothesis that already obese women with the Trp64Arg polymorphism of the beta3-adrenergic receptor gene have lower daily energy expenditure, altered lipolysis, and increased abdominal obesity. On the other hand, the lower RMR in never-obese women suggests that the obese state may mask a moderate effect of the Trp64Arg variant on energy expenditure. Although these results need to be confirmed in other populations, the obese state may have been a confounding factor in previous studies of the beta3-adrenoceptor Trp64Arg variant and energy expenditure.

Arginine↗
PubMed2002

A unique defect in the regulation of visceral fat cell lipolysis in the polycystic ovary syndrome as an early link to insulin resistance.

The etiology of polycystic ovary syndrome (PCOS) is unknown. However, PCOS has a strong resemblance to the insulin resistance (metabolic) syndrome, where an increased rate of visceral fat cell lipolysis is believed to play a pathophysiological role. We hypothesized that primary defects in visceral lipolysis might also exist in PCOS. Ten young, nonobese, and otherwise healthy PCOS women were compared with 13 matched control women. In vitro lipolysis regulation and stoichiometric properties of the final step in lipolysis activation, namely the protein kinase A (PKA)-hormone sensitive lipase (HSL) complex, were investigated in isolated visceral (i.e., omental) fat cells. Body fat distribution and circulating levels of insulin, glucose, and lipids were normal in PCOS women. However, in vivo insulin sensitivity was slightly decreased (P = 0.03). Catecholamine-induced adipocyte lipolysis was markedly (i.e., about twofold) increased in PCOS women due to changes at the postreceptor level, although there was no change in the antilipolytic properties of visceral fat cells. Western blot analyses of visceral adipose tissue showed twofold increased levels of the catalytic and the regulatory Ialpha components of PKA. In contrast, the regulatory RIIbeta component of PKA was almost 50% decreased in visceral adipose tissue in PCOS women. Recent studies on genetically modified mice have shown that a similar transition in the regulatory PKA units induces an increased lipolytic response to catecholamines. Further analysis showed that the level of HSL-short, an enzymatically inactive splice form of HSL, was decreased in PCOS (P < 0.01). The altered lipolysis in PCOS is different from that observed in visceral fat cells in the insulin resistance syndrome that occurs at the level of adrenergic receptors. We concluded that increased catecholamine-induced lipolysis in visceral fat cells may be due to unique alterations in the stoichiometric properties of the adipose PKA-HSL holoenzymes. This could be an early and possibly primary lipolysis defect in PCOS.

Adipocytes↗
PubMed2004

Adiponectin gene polymorphisms and adiponectin levels are independently associated with the development of hyperglycemia during a 3-year period: the epidemiologic data on the insulin resistance syndrome prospective study.

The plasma concentration of the adipocyte-derived peptide adiponectin is decreased in patients with obesity and type 2 diabetes. The adiponectin gene is located on chromosome 3q27, where a diabetes susceptibility locus has been mapped. Adiponectin gene polymorphisms (single nucleotide polymorphisms [SNPs]) have been associated with BMI, insulin sensitivity, and type 2 diabetes in some cross-sectional studies. Our aim was to assess the contribution of these SNPs in the development of features of the insulin resistance syndrome in a 3-year prospective study in approximately 4,500 French Caucasian subjects from the Epidemiologic Data on the Insulin Resistance Syndrome (DESIR) cohort. For subjects who were normoglycemic at baseline, the 3-year risk of becoming hyperglycemic (diabetes or impaired fasting glucose) was affected by two SNPs: G-11391A and T45G. For G-11391A, the risk was increased in GA carriers (odds ratio [OR] adjusted for sex [versus GG] = 1.60 [95% CI 1.16-2.20]; P = 0.004). For T45G, it was increased in GG carriers (OR [versus TT] = 2.71 [1.31-5.60]; P = 0.007). After 3 years, GG subjects had a greater increase in BMI (P = 0.009) and waist-to-hip ratio (P = 0.007). Adiponectin levels at baseline were associated with the development of hyperglycemia (P = 0.005), but the predictive effects on the risk for hyperglycemia were independent of adiponectin genotypes. In conclusion, in the DESIR study, variations at the adiponectin locus affect body weight gain, body fat distribution, and onset of hyperglycemia, as well as adiponectin levels. Adiponectin gene SNPs may have several phenotypic effects that co-occur with the development of the metabolic syndrome.

Adiponectin↗
PubMed2005

Adiponectin is lower among African Americans and is independently related to insulin sensitivity in children and adolescents.

Adiponectin is inversely related to adiposity and positively correlated with insulin sensitivity (S(i)). Sparse data exist on the contributions of ethnicity and body fat distribution to variance in serum adiponectin. Hypotheses tested were that adiponectin would be lower in African Americans compared with Caucasians; that adiponectin would be inversely related to central, not peripheral, fat; that adiponectin would be positively associated with S(i); and that baseline adiponectin would predict change in S(i) over 2 years in 150 African-American and Caucasian youth. Multiple linear regression modeling showed that adiponectin was lower in African-American versus Caucasian children (adjusted means 10.8 +/- 0.5 vs. 12.3 +/- 0.5 microg/ml, respectively; P < 0.05); inversely related to trunk fat (P < 0.05); and positively related to limb fat (P < 0.01). Addition of the acute insulin response to glucose to the model eliminated the significance of ethnicity. S(i), which was positively related to adiponectin (P < 0.05), was lower in African Americans (P < 0.001) and girls (P < 0.05). Baseline adiponectin did not predict change in S(i) over 2 years. In conclusion, adiponectin was positively correlated with S(i), inversely related to central fat, and positively related to peripheral fat. In addition, higher acute insulin response to glucose explained lower adiponectin among African-American children.

Adipose Tissue↗
PubMed1991

Kelly West Lecture. Primary prevention of type II diabetes mellitus.

A useful paradigm for developing a public health strategy for combating chronic diseases consists of three phases: observational epidemiological studies, first cross-sectional and then prospective; intervention trials; and, finally, public health action. Although the field of cardiovascular epidemiology is well advanced into the third phase, i.e., public health action, the field of diabetes epidemiology is at least a generation behind and has only recently entered the phase of prospective observational studies. Part of the reason for this lag may be that, unlike cardiovascular disease, non-insulin-dependent (type II) diabetes has not been traditionally viewed as an epidemic, thereby detracting from a sense of urgency about the disease. Although this perspective may be appropriate for white populations, data from around the world make it increasingly apparent that type II diabetes has indeed reached epidemic proportions in non-white populations. Prospective studies are needed to firmly establish risk factors on which public health actions can be confidently based. Although anthropometric and metabolic risk factors such as obesity, body fat distribution, and circulating glucose and insulin concentrations are becoming well established as risk factors for type II diabetes, much less is known about behavioral risk factors. These latter risk factors are especially important because they are often amenable to public health action. There are preliminary data suggesting that decreased physical activity and increased fat consumption may be behavioral risk factors for diabetes. Decreased total energy intake, reflecting either low levels of physical activity or an intrinsically low metabolic rate, perhaps genetic in origin, may also be a diabetes risk factor. Unlike the field of cardiovascular epidemiology, in which there is already a critical mass of intervention trials on primary prevention, such trials are essentially nonexistent in the field of diabetes epidemiology; they are urgently needed. Although the notion of a single gene causing diabetes is clearly simplistic, there is a reasonable expectation that genetic markers can be identified that would be useful in screening for genetic susceptibles, at least in selected predisposed populations. Such markers could then be used to identify target populations for primary-prevention trials and public health action. Although primary-prevention trials should not be deferred until genetic markers are available, these two research paths may someday converge and genetic markers may come to play an important role in screening individuals as part of a comprehensive public health strategy. Numerous trial designs should be considered for testing hypotheses about the primary prevention of type II diabetes. These include single risk factor, multiple risk factor, and factorial designs.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1992

Greater effect of glycemia on incidence of hypertension in women than in men.

OBJECTIVE: In subjects with NIDDM, diabetic women have a greater relative excess of CHD relative to nondiabetic women than do diabetic men relative to nondiabetic men. This excess in diabetic women is explained partially by the particularly atherogenic pattern of lipoproteins in this group. We hypothesize that diabetic women also may have a higher incidence of hypertension than diabetic men. RESEARCH DESIGN AND METHODS: We examined the effect of NIDDM and IGT relative to NGT on the incidence of hypertension separately in men (n = 844) and women (n = 618) in the 8-yr follow-up of the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. RESULTS: Women had a greater risk of hypertension with worsening glucose tolerance (RR NIDDM/NGT = 2.65 and RR IGT/NGT = 1.94) compared with men (RR NIDDM/NGT = 1.61 and RR IGT/NGT = 0.91). Controlling for other possible confounding variables such as age, obesity, body fat distribution, and fasting insulin concentration did not alter the interaction of sex and glycemia on incidence of hypertension. CONCLUSIONS: The especially increased risk of hypertension in women with abnormal glucose tolerance may explain partly the high risk of CHD in this group.

Blood Glucose↗
PubMed1996

Nondiabetic Mexican-Americans do not have reduced insulin responses relative to nondiabetic non-Hispanic whites.

OBJECTIVE: To study why Mexican-Americans have a threefold increase in NIDDM relative to non-Hispanic whites. The etiology of NIDDM is still controversial, with both insulin resistance and decreased insulin secretion proposed as precursors of NIDDM. RESEARCH DESIGN AND METHODS: We examined possible ethnic differences in fasting insulin (as a marker of insulin resistance) and change in insulin-to-change in glucose ratio (delta I30:delta G30) during the first 30 min after oral glucose ingestion (as a marker of abnormal whites from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Fasting insulin and delta I30:delta G30 were evaluated as continuous variables. RESULTS: Mexican-Americans had increased insulin concentrations at fasting and 30, 60, and 120 min after an oral glucose load as well as an increased 0- to 30-min increment in insulin and delta I30:delta G30 relative to non-Hispanic whites. These results remained unchanged after adjustment for age, sex, obesity, body fat distribution, and glucose tolerance. CONCLUSIONS: These results suggest that increased insulin resistance rather than decreased insulin secretion is characteristic of nondiabetic Mexican-Americans, a high-risk population for NIDDM.

Blood Glucose↗
PubMed1999

Insulin sensitivity in subjects with type 2 diabetes. Relationship to cardiovascular risk factors: the Insulin Resistance Atherosclerosis Study.

OBJECTIVE: Among nondiabetic subjects, insulin resistance has been associated with increased cardiovascular risk factors, including dyslipidemia, hypertension, impaired fibrinolysis, and coagulation. Less is known about the relationship between insulin resistance and cardiovascular risk factors in subjects with type 2 diabetes. RESEARCH DESIGN AND METHODS: To examine this issue, we determined insulin sensitivity (SI) in 479 type 2 diabetic subjects by minimal model analyses of frequently sampled intravenous glucose tolerance tests in the Insulin Resistance Atherosclerosis Study (IRAS), a large multicenter study of insulin sensitivity and cardiovascular disease in African-Americans, Hispanics, and non-Hispanic whites. We defined insulin-sensitive subjects as having SI > or = 1.61 x 10(-4) min-1.microU-1.ml-1 (above median in nondiabetic subjects of all ethnic groups in the IRAS). Using this definition, only 37 type 2 diabetic subjects were insulin sensitive, and the remaining 442 were insulin resistant. RESULTS: After adjustment for age, sex, ethnicity, and clinic, insulin resistance was significantly correlated with total triglycerides, VLDL cholesterol, VLDL triglyceride, fibrinogen, PAI-1, and fasting glucose, and was inversely correlated with HDL cholesterol level and LDL size. Carotid intimal-medial thickness was greater in insulin-resistant than in insulin-sensitive subjects, but this difference was not statistically significant. After further adjustment for waist circumference (marker of visceral adiposity), insulin-resistant subjects continued to have higher plasminogen activator inhibitor 1 and VLDL triglyceride levels, lower HDL cholesterol levels, and smaller LDL particle size than did insulin-sensitive subjects. After further adjustment for fasting glucose levels, these results were very similar. CONCLUSIONS: We conclude that insulin-resistant type 2 diabetic subjects have more atherogenic cardiovascular risk factor profiles than insulin-sensitive type 2 diabetic subjects and that this is only partially related to increased obesity and an adverse body fat distribution.

Black or African American↗
PubMed2006

Abdominal adiposity is a stronger predictor of insulin resistance than fitness among 50-95 year olds.

OBJECTIVE: Physical inactivity and increased adiposity contribute to insulin resistance; less is known, however, about the relative contributions of these factors in older adults. The aim of this study was to determine whether cardiovascular fitness, whole-body adiposity, or abdominal adiposity is the strongest predictor of insulin resistance into old age. RESEARCH DESIGN AND METHODS: Subjects included 407 men and women aged 50-95 years (means +/- SD 69 +/- 11 years). Insulin resistance was estimated using the insulin sensitivity index (ISI) of Matsuda and DeFronzo [ISI = 10,000/square root of (fasting glucose x fasting insulin) x (mean glucose x mean insulin during an oral glucose tolerance test); lower ISI = greater insulin resistance]. Fitness was determined with a treadmill maximal oxygen consumption (Vo(2max)) test. Whole-body adiposity measures included BMI and percent fat by dual-energy X-ray absorptiometry or hydrodensitometry; abdominal adiposity was estimated by waist circumference. RESULTS: Waist circumference was the strongest independent correlate of ISI (r = -0.52, P < 0.0001), explaining 28% of the variance when controlling for sex, BMI, percent fat, and Vo(2max). BMI (r = -0.45), percent fat (r = -0.40), and Vo(2max) (r = 0.22) independently predicted ISI (all P < 0.0001); however, after controlling for waist circumference, only Vo(2max) remained significant (r = 0.13, P = 0.009). CONCLUSIONS: Adiposity and fitness continue to be significant predictors of insulin sensitivity into old age, with abdominal obesity being the most important single factor. These findings support the measurement of waist circumference to assess health risk among older adults.

Abdominal Fat↗