QUICKI Index Research Articles

Resistin, insulin sensitivity and markers of inflammation in a cohort of Romanian patients under combined antiretroviral therapy

Methods We performed a transversal study that used the following inclusion criteria: non-diabetic patients with documented HIV infection, undergoing stable cART for at least 6 months. Clinical, metabolic, inflammatory and immuno-virological patterns were assessed (age, sex, body mass index, HIV load, actual and nadir CD4, duration of HIV infection and antiretroviral therapy, lipid panel, C-reactive protein CRP). Resistin levels were evaluated using KAPME Biosource EASIA. In order to test the sensitivity to insulin we used the QUICKI index, the best surrogate marker after glucose clamp index. Parametric and non-parametric variables were described using means (±Standard Deviation SD) and medians (Interquartile Ratio IQR), respectively.

Hawthorne effect with transient behavioral and biochemical changes in a randomized controlled sleep extension trial of chronically short-sleeping obese adults: implications for the design and interpretation of clinical studies.

ObjectiveTo evaluate the effects of study participation per se at the beginning of a sleep extension trial between screening, randomization, and the run-in visit.DesignSubjects were screened, returned for randomization (Comparison vs. Intervention) after 81 days (median), and attended run-in visit 121 days later.SettingOutpatient.PatientsObese (N = 125; M/F, 30/95; Blacks/Whites/Other, N = 73/44/8), mean weight 107.6±19.7 kg, <6.5 h sleep/night.InterventionNon-pharmacological sleep extension.MeasurementsSleep duration (diaries and actigraphy watch), sleep quality (Pittsburgh Sleep Quality Index), daily sleepiness (Epworth Sleepiness Scale), fasting glucose, insulin and lipids.ResultsPrior to any intervention, marked improvements occurred between screening and randomization. Sleep duration increased (diaries: 357.4 ±51.2 vs. 388.1±48.6 min/night; mean±SD; P<0.001 screening vs. randomization; actigraphy: 344.3 ±41.9 vs. 358.6±48.2 min/night; P<0.001) sleep quality improved (9.1±3.2 vs. 8.2±3.0 PSQI score; P<0.001), sleepiness tended to improve (8.9±4.6 vs. 8.3±4.5 ESS score; P = 0.06), insulin resistance decreased (0.327±0.038 vs. 0.351±0.045; Quicki index; P<0.001), and lipids improved, except for HDL-C. Abnormal fasting glucose (25% vs. 11%; P = 0.007), and metabolic syndrome (42% vs. 29%; P = 0.007) both decreased. In absence of intervention, the earlier metabolic improvements disappeared at the run-in visit.LimitationsRelatively small sample size.ConclusionsImprovements in biochemical and behavioral parameters between screening and randomization changed the “true” study baseline, thereby potentially affecting outcome. While regression to the mean and placebo effect were considered, these findings are most consistent with the “Hawthorne effect”, according to which behavior measured in the setting of an experimental study changes in response to the attention received from study investigators. This is the first time that biochemical changes were documented with respect to the Hawthorne effect. The findings have implications for the design and conduct of clinical research.Trial RegistrationClinicalTrials.gov NCT00261898.

Association between prehypertension, metabolic and inflammatory markers, decreased adiponectin and enhanced insulinemia in obese subjects.

BackgroundObesity is associated with development of the cardiorenal metabolic syndrome, which is a constellation of risk factors, such as insulin resistance, inflammatory response, dyslipidemia, and high blood pressure that predispose affected individuals to well-characterized medical conditions such as diabetes, cardiovascular and kidney chronic disease. The study was designed to establish relationship between metabolic and inflammatory disorder, renal sodium retention and enhanced blood pressure in a group of obese subjects compared with age-matched, lean volunteers.MethodsThe study was performed after 14 h overnight fast after and before OGTT in 13 lean (BMI 22.92 ± 2.03 kg/m2) and, 27 obese (BMI 36.15 ± 3.84 kg/m2) volunteers. Assessment of HOMA-IR and QUICKI index were calculated and circulating concentrations of TNF-α, IL-6 and C-reactive protein, measured by immunoassay.ResultsThe study shows that a hyperinsulinemic (HI: 10.85 ± 4.09 μg/ml) subgroup of well-characterized metabolic syndrome bearers-obese subjects show higher glycemic and elevated blood pressure levels when compared to lean and normoinsulinemic (NI: 5.51 ± 1.18 μg/ml, P < 0.027) subjects. Here, the combination of hyperinsulinemia, higher HOMA-IR (HI: 2.19 ± 0.70 (n = 12) vs. LS: 0.83 ± 0.23 (n = 12) and NI: 0.98 ± 0.22 (n = 15), P < 0.0001) associated with lower QUICKI in HI obese when compared with LS and NI volunteers (P < 0.0001), suggests the occurrence of insulin resistance and a defect in insulin-stimulated peripheral action. Otherwise, the adiponectin measured in basal period was significantly enhanced in NI subjects when compared to HI groups (P < 0.04). The report also showed a similar insulin-mediated reduction of post-proximal urinary sodium excretion in lean (LS: 9.41 ± 0.68% vs. 6.38 ± 0.92%, P = 0.086), and normoinsulinemic (NI: 8.41 ± 0.72% vs. 5.66 ± 0.53%, P = 0.0025) and hyperinsulinemic obese subjects (HI: 8.82 ± 0.98% vs. 6.32 ± 0.67%, P = 0.0264), after oral glucose load, despite elevated insulinemic levels in hyperinsulinemic obeses.ConclusionIn conclusion, this study highlights the importance of adiponectin levels and dysfunctional inflammatory modulation associated with hyperinsulinemia and peripheral insulin resistance, high blood pressure, and renal dysfunction in a particular subgroup of obeses.

Effects of supplementation with omega-3 on insulin sensitivity and non-esterified free fatty acid (NEFA) in type 2 diabetic patients.

The aim of this study was to determine the role of omega-3 supplementation on NEFA concentration, insulin sensitivity and resistance, and glucose and lipid metabolism in type 2 diabetic patients. Forty-four type 2 diabetic patients were randomly recruited into two groups. Group A received 4 g/day omega-3 soft gels, and group B received a placebo for 10 wks. Blood samples were collected after 12-h fast. Physical activity records, three-day food records, and anthropometric measurements were obtained from all participants at the beginning and end of the study. Omega-3 supplementation caused a significant reduction in NEFA in the intervention group compared with the placebo group (P = 0.009). Additionally, the administration of omega-3 resulted in significantly greater changes (Diff) for the intervention group in various parameters, such as insulin and Quicki indices compared with the placebo group (P < 0.05). Omega-3 fatty acid supplementation in type 2 diabetic patients improved insulin sensitivity, probably due to the decrease in NEFA concentrations.

Upper-body obese women are resistant to postprandial stimulation of protein synthesis

Upper-body, i.e. visceral, obesity is associated with insulin resistance and impaired protein synthesis. It is unclear whether postprandial stimulation of protein synthesis is affected by body fat distribution. We investigated the postprandial protein anabolic response in a cohort of obese women. Participants were studied after an overnight fast and after a mixed meal, grouped as upper-body obese (UBO, waist-to-hip ratio, WHR, >0.85, n = 6) vs. lower-body obese (LBO, WHR <0.80, n = 7). Lipid and carbohydrate metabolism were assessed by measurements of plasma free fatty acids (FFA), insulin and glucose plasma concentrations, and calculation of the Quicki index from fasting glucose and insulin values. Different labels of stable isotopes of phenylalanine were administered intravenously and orally, and leg and whole-body protein breakdown and synthesis were calculated from phenylalanine/tyrosine isotopic enrichments in femoral arterial and venous blood, using equations for steady-state kinetics. Data are denoted as mean ± SD. Age (38 vs. 40, p = 0.549) and body-mass index (33.7 ± 1.9 vs. 35.0 ± 1.8, p = 0.241) were similar in both groups. UBO subjects had more visceral fat (p = 0.002) and higher fat-free body mass (FFM) (p = 0.015). Plasma insulin concentrations were greater in UBO than LBO women (p = 0.013), and UBO were less insulin sensitive (Quicki = 0.32 ± 0.01 vs. 0.36 ± 0.02, p = 0.005). Protein kinetics across the leg were not different between groups. Fasting whole body protein balance was similarly negative in both groups (UBO -6.5 ± 2.4 vs. LBO -7.6 ± 0.9 μmol/kgFFM/h, p = 1.0). Postprandially, whole body protein balance became less positive in UBO than in LBO (14.8 ± 3.7 vs. 20.2 ± 3.7 μmol/kgFFM/h, p = 0.017). Whole-body protein balance following a meal is less positive in upper-body obese, insulin-resistant, women than in lower-body obese women.

Variability of formulas to assess insulin sensitivity and their association with the Matsuda index.

To assess the individual variability of HOMA and QUICKI indexes for the assessment of insulin resistance, using three fasting blood samples obtained within 30 minutes. Data from 80 participants aged 41.5 ± 15 years (26 females), who underwent an oral glucose tolerance test to calculate Matsuda index, were used. Every participant had three fasting blood samples obtained within 30 minutes and four blood samples obtained at 30, 60, 90 and 120 minutes after a 75 g oral glucose load. Insulin and glucose were measured in each sample. HOMA and QUICKI indexes were calculated using the nine possible combinations of the three fasting blood samples. Matsuda index was calculated with all samples obtained. Median values of HOMA-IR, HOMA-β, QUICKI and Matsuda indexes were 1.9, 117.9, 0.35 and 3.71 arbitrary units, respectively. The individual variation coefficients of HOMA-IR, HOMA-β and QUICKI were 11.8 (7.8-18.9), 15 (10.2-22.9) and 1.8 (8.8-21.9) % respectively. When compared with Matsuda index, the R squared values of HOMA-IR, HOMA-β and QUICKI were 0.46, 0.2 and 0.71, respectively. Among fasting indexes for insulin resistance, QUICKI had the lower variation coefficient and the higher correlation with Matsuda index.

Beneficial Effects of Fresh and Fermented Kimchi in Prediabetic Individuals

Background: With the increased incidence of diabetes mellitus, the importance of early intervention in prediabetes has been emphasized. We previously reported that fermented kimchi, a traditional Korean food, reduced body weight and improved metabolic factors in overweight participants. We hypothesized that kimchi and its fermented form would have beneficial effects on glucose metabolism in patients with prediabetes. Methods: A total of 21 participants with prediabetes were enrolled. During the first 8 weeks, they consumed either fresh (1-day-old) or fermented (10-day-old) kimchi. After a 4-week washout period, they switched to the other type of kimchi for the next 8 weeks. Results: Consumption of both types of kimchi significantly decreased body weight, body mass index, and waist circumference. Fermented kimchi decreased insulin resistance, and increased insulin sensitivity, QUICKI and disposition index values (p = 0.004 and 0.028, respectively). Systolic and diastolic blood pressure (BP) decreased significantly in the fermented kimchi group. The percentages of participants who showed improved glucose tolerance were 9.5 and 33.3% in the fresh and fermented kimchi groups, respectively. Conclusions: Consumption of kimchi had beneficial effects on glucose metabolism-related and anthropometric factors in participants with prediabetes. Fermented kimchi had additional effects on BP and insulin resistance/sensitivity. The percentage of participants who showed improvement in glucose tolerance was high in the fermented kimchi group.

Role of plasminogen activator inhibitor and free fatty acids in diagnosis of insulin resistance in patients with myocardial infarction

Purpose: To access the insulin resistance markers dynamics in ST-segment elevation patients with MI with presented and non-presented T2DM in acute and post-acute rehabilitation periods. Methods: 95 patients with myocardial infarction and 60 patients with MI and associated T2DM were included in the study; the control group consisted of 30 healthy subjects. The concentration of serum FFA, glucose, C-peptide and insulin were measured on the 1st and 12th days of the study. MI was diagnosed according to the 2007 National Scientific Cardiology Society. The study design was approved by the Institutional Review Board. The insulin resistance level was estimated using a mathematical model incorporating fasting serum insulin and glucose measurement with the QUICKI calculation. The results were statistically processed using non-parametric criteria; differences were considered to be statistically significant in p < 0.05. Results: Blood glucose level increased in the Group 1 and on the 1st day after MI onset. An elevation of glucose level was noticed in the Group 2 during the whole follow-up period, whereas in the Group 1 blood glucose level decreased on the 12th day. Postprandial glucose level increased in the Group 2 in comparison with the control values on the 12th day from the MI onset. In contrast, fasting serum insulin and C-peptide level tended to increase in both groups on the 1st and 12th days from the MI onset. Postprandial insulin level raised equally in both groups compared to the control group. In the Group 1, the QUICKI indices were 0,316±0.005 and 0,319±0.005 on the 1st and 12th days after the MI onset, respectively, and they were interpreted as breakpoint values between severe and moderate IR. In the Group 2, the QUICKI indices were 0,296±0.009 and 0,300±0.005, that verified a pronounced tissue insulin resistance. FFA levels in the Group 1 and in the Group 2 exceeded the control group values. PAI-1 concentration was higher in the Group 1 and higher in the Group 2 compared to the control group on the 1st day. In addition, PAI-1 concentration significantly reduced in both groups on the 12th day. Postprandial insulin positively correlated to FFA levels (R=0,47, p=0.02) and QUICKI index negatively correlated to FFA levels (R=-0,229, p=0,006). Moreover, a negative correlation between PAI-1 concentration and QUICKI index was reported in Group 2 and in Group 1 (R= -0,77, p=0,005; R= -0,47, p=0,005, respectively). Conclusion: Elevated FFA and PAI-1 levels are significant indicators of impaired insulin sensitivity under the conditions of acute MI compared to the postprandial glycemia and insulinemia.

Chemotherapy for testicular cancer induces acute alterations in diastolic heart function

Background:After treatment with cisplatin-based chemotherapy for testicular cancer (TC), patients have higher prevalence of cardiovascular complications after long-term follow up. Little is known about acute cardiovascular effects of cisplatin-based chemotherapy. The aim of this study was to explore acute effects of chemotherapy on cardiac function in patients treated for TC.Methods:Fourteen TC patients (age 34.6±12.3 years) were studied before and 3 months after start with cisplatin-based chemotherapy. Cardiac function was assessed with magnetic resonance imaging. Fasting glucose and insulin levels were measured and insulin sensitivity, reflected by the quantitative insulin sensitivity index (Quicki index), was calculated.Results:Left ventricular (LV) end-diastolic volume and LV stroke volume (SV) significantly decreased from 192±27 to 175±26 ml (P<0.05) and 109±18 to 95±16 ml (P<0.05), respectively. The ratio of early and atrial filling velocities across the mitral valve, a parameter of diastolic heart function, decreased after chemotherapy from 1.87±0.43 to 1.64±0.45 (P<0.01). Metabolic parameters were unfavourably changed, reflected by a decreased Quicki index, which reduced from 0.39±0.05 to 0.36±0.05 (P<0.05).Conclusion:Chemotherapy for TC induces acute alterations in diastolic heart function, paralleled by unfavourable metabolic changes. Therefore, early after chemotherapy, metabolic treatment may be indicated to possibly reduce long-term cardiovascular complications.

SAT0080 Early Rheumatoid Arthritis Patients without Treatment: Baseline Asessment of Insulin Resistance and Cytokines

ObjectivesTo analyze insulin resistance (IR), inflammatory cytokines, adipokines and clinical and laboratory characteristics in patients with early rheumatoid arthritis (ERA) who have not received any treatment for their disease.MethodsThis is...

AB0316 Changes of adipokine serum levels after il-6 receptor blockade with tocilizumab in patients with rheumatoid arthritis

BackgroundImmune dysregulation and systemic inflammation are integral to the development of accelerated atheromatosis in rheumatoid arthritis (RA), mediated by various cytokines. Imbalance of haemostasis, as evidenced by increased levels of...

Insulin resistance, serum insulin and HOMA-R

The authors really appreciate the comments by Tomoyuki Kawada on their paper entitled ‘‘The effect of etanercept on hepatic fibrosis risk in patients with non-alcoholic fatty liver disease, metabolic syndrome and psoriasis’’ [1]. For Kawada [2], HOMA-R and serum insulin show equivalent efficacy in detecting insulin resistance, whereas it may be more difficult to calculate HOMA-R in subjects with increased fasting plasma glucose. Therefore, the homeostasis model assessment for insulin resistance could be substituted simply by serum insulin, with no need for data on plasma glucose [2]. This is a sharable point of view, however, the study reported by the author refers specifically to a wide male population without a current history of treatment for diabetes, hypertension, dyslipidemia, hyperuricemia, coronary, and/or cerebrovascular disease. Thus, when Kawada stated that both HOMA-R and serum insulin are equivalent in detecting insulin resistance, he specifically refers to apparently healthy subjects. However, conversely to population with no remarkable medical conditions considered by Kawada, our case series includes subjects with psoriasis, metabolic syndrome and NAFLD. In our opinion, in such a setting of patients, more than one marker of insulin resistance should be taken into consideration. Regarding the second query, focusing on the use of QUICKI and HOMA indexes in our study, we have to specify that in our retrospective analysis we selected patients with concomitant psoriasis, metabolic syndrome and NAFLD who had received etanercept or PUVA, and did not base our selections exclusively on FPG values. It’s true that in our retrospective analysis, the FPG values of included patients ranged from 73 to 122 mg/dl, but this was simply a matter of chance since we did not preventively exclude patients with FPG [ 140 mg/dl, as speculated by Kawada. Therefore, given FPG values \140 mg/dl, we deliberately decided to use both HOMA and QUICKI [3]. One of the limiting factors of our study was precisely that we did have not patients with FPG [ 140 mg/dl, because of its retrospective nature. Finally, the authors acknowledge the suggestion to directly assess the risk of hepatic fibrosis in further advanced studies.

Comparing the effects of inorganic nitrate and allopurinol in renovascular complications of metabolic syndrome in rats: role of nitric oxide and uric acid.

IntroductionThe epidemic of metabolic syndrome is increasing worldwide and correlates with elevation in serum uric acid and marked increase in total fructose intake. Fructose raises uric acid and the latter inhibits nitric oxide bioavailability. We hypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome and treatment of hyperuricemia or increased nitric oxide may improve it.Material and methodsTwo experiments were performed. Male Sprague-Dawley rats were fed a control diet or a high-fructose diet to induce metabolic syndrome. The latter received either sodium nitrate or allopurinol for 10 weeks starting with the 1st day of fructose to evaluate the preventive role of the drugs or after 4 weeks to evaluate their therapeutic role.ResultsA high-fructose diet was associated with significant (p < 0.05) hyperuricemia (5.9 ±0.5 mg/dl), hypertension (125.2 ±7.8 mm Hg), dyslipidemia and significant decrease in tissue nitrite (27.4 ±2.01 mmol/l). Insulin resistance, as manifested by HOMAIR (20.6 ±2.2) and QUICKI (0.23 ±0.01) indices, as well as adiposity index (12.9 ±1.1) was also significantly increased (p < 0.1). Sodium nitrate or allopurinol was able to reverse these features significantly (p < 0.05) in the preventive study better than the therapeutic study.ConclusionsFructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid. Either sodium nitrate or allopurinol can prevent this pathological condition by different mechanisms of action.

Hyperglycemia and lower diet quality in pregnant overweight women and increased infant size at birth and at 13 months of age — STEPS study

AimsTo study whether maternal overweight and/or hyperglycemia combined with life-style factors in healthy women predisposes to adverse pregnancy or infant health outcomes, such as differences in growth. MethodsAt 26–28weeks of gestation 82 overweight pregnant women (prepregnancy BMI≥25kg/m2) and 67 normal weight pregnant women (prepregnancy BMI<25kg/m2) participating to STEPS study attended 2-hour oral glucose tolerance test (OGTT) with measurement of plasma glucose and insulin and calculation of HOMA, QUICKI and Matsuda ISI indices. Birth weights and lengths were obtained from hospital records and weights and heights at 13months from study visits. Maternal physical activity and diet quality were studied with questionnaires. ResultsGlucose concentrations were higher in overweight non-diabetic women (0h=4.9, 1h=7.7, 2h=6.2mmol/l, n=80) than normal weight women (0h=4.5, 1h=6.8, 2h=5.6mmol/l, all P<0.05, n=66) as were insulin concentrations at baseline (12.3 vs. 9.0mU/l, P<0.05), but not later (1h=88.1 vs. 72.8mU/l; 2h=63.5 vs. 55.5mU/l, both P>0.05). Insulin resistance was higher and sensitivity lower (P<0.05 for all) in overweight than in normal weight women. The offspring of overweight mothers were 273g heavier at birth and 700g heavier at 13months of age than the offspring of normal weight women (P<0.001). Normal weight women had preferable diet quality (P=0.023). No differences were seen in self-reported physical activity between overweight and normal weight women. ConclusionsMaternal prepregnancy overweight increases risk of hyperglycemia in late-pregnancy and increased infant size at birth and 13months possibly predisposing the infant to health risks later in life.

Repeated analysis of estimated insulin resistance using the HOMAIR index in nondiabetic patients on peritoneal dialysis and its relationship with cardiovascular disease and mortality.

Terminal chronic renal failure patients show early insulin resistance (IR), characterised by alterations in the hydrocarbon metabolism and hyperinsulinaemia generally associated with dyslipidaemia and a proinflammatory condition. Cardiovascular disease (CVD) is the main cause of mortality in patients on dialysis. There is a strong association between IR, hyperinsulinism and CV disease. The objective of this study was to evaluate the effect of peritoneal dialysis (PD) on IR and its effects on the subsequent CVD morbidity and mortality in nondiabetic uraemic patients. It involved 69 nondiabetic patients on PD, 35 incident patients (≤ 3 months on PD) and 34 prevalent patients (>3 months on PD), with 2 estimated insulin resistance measurements 12 months apart using the insulin resistance index (HOMAIR). The mean HOMAIR value in incident patients was 1.8 ± 1.3 and 2.2 ± 2.1 at baseline situation and at 12 months respectively (not significant [NS]). In prevalent patients these values were 2.3 ± 1.3 and 2.5 ± 2.2 (NS). In our study, the mean glucose, insulin and IR concentrations measured by the HOMAIR and QUICKI indexes (the latter being a quantitative control for insulin sensitivity control) were similar at baseline situation and the following year, in both incident and prevalent patients. We did not find any significant differences in relation to CVD comorbidity, ischaemic heart disease, heart failure or cerebrovascular or peripheral comorbidity neither in the HOMAIR index or insulin levels. To conclude, nondiabetic patients on PD do not display a significant increase in HOMAIR levels and this remains the case over time when on dialysis. This, in turn, suggests that PD is not an IR risk factor. The fact that the IR indexes are not associated with CVD morbidity or mortality seems to suggest that this is a less significant factor in the field of PD.

Relationship of raised serum total and protein bound sialic acid levels with hyperinsulinemia and indices of insulin sensitivity and insulin resistance in non-diabetic normotensive obese subjects

AimsObesity is known to be associated with cardiovascular disease and interaction between inflammation and insulin resistance is reported to enhance the cardiovascular risk in these subjects. The present study was designed to assess indices of insulin sensitivity, insulin resistance and sialic acid levels and their association in non-diabetic normotensives obese subjects. Materials and methodsThe present study was conducted in 30 obese male subjects and results were compared with 30 subjects with normal body weight. Insulin, total sialic acid and protein bound sialic acid were estimated in all the subjects. Insulin resistance was calculated by using Homeostatic Model Assessment-insulin resistance formula. Insulin sensitivity was assessed by quantitative insulin check index and insulin sensitivity index. ResultsInsulin resistance, serum total and protein bound sialic acid levels were significantly increased in obese cases as compared to non-obese controls. Total sialic acid showed significant positive correlation with HOMA-IR (p<0.01), BMI (p<0.01), waist and hip circumference (p<0.01) and negative correlation with QUICKI (p<0.01) and insulin sensitivity index (p=0.018). There was no significant correlation between protein bound sialic acid and indices of insulin resistance and insulin sensitivity. ConclusionSialic acid levels are elevated in obese subjects and its association with insulin resistance and reduced insulin sensitivity may enhance the cardiovascular risk in these subjects.

Effect of Anti-TNF Therapy on Resistance to Insulin in Patients with Rheumatoid Arthritis

Objective: To evaluate the effect of anti-TNF therapy on resistance to insulin in patients with rheumatoid arthritis (RA) compared with patients with RA being treated with non-biological DMARDs. Methods: Inactive patients diagnosed with RA (ACR 1987 criteria) (DAS 28 2.6) were included, being treated with anti-tumor necrosis factor inhibitors (anti-TNF) (cases) and non-biological disease-modifying anti-rheumatic drugs (DMARD) (controls), without risk factors for insulin resistance (administration of steroids, body mass index > 25 kg/m2, diabetes mellitus or use of glucose lowering agents, systemic arterial hypertension or use of anti-hypertensive drugs, triglycerides > 150 mg/dl, hypercholesterolemia > 200 mg/dl, high-density lipoproteins 40 mg/dl in men and 50 mg/in women, or with lipids lowering agents, waist measurement > 88 cm in women and > 102 cm in men). We used HOMA (Homeostasis Model Assessment) to determine insulin resistance in both groups, HOMA being defined as >1 and sensitivity to insulin using QUICKI (Insulin Sensitivity Check Index), ≥0.38 being considered as normal. The Mann Whitney U was used for the statistical analysis. Results: A total of 28 patients, 15 being treated with non-biological DMARDs and 13 with anti-TNF therapy, were evaluated; 89.7%, of which were women. Average age: 43.5 (range 21 - 62); the average HOMA index of the non-biological DMARD group was 1.58 (range 0.7 - 5.4), compared with patients treated with anti-TNF therapy, 1.18 (range 0.2 - 4.3) (P = 0.5). The average QUICKI index was 0.36 (range 0.30 - 0.42) in patients treated with non-biological DMARD, compared with0.37 inpatients treated with anti-TNF therapy (range 0.30 - 0.51) (P = 0.8). Conclusion: Resistance to insulin manifested itself in both groups, although there was a greater trend of less insulin resistance and greater sensitivity in the anti-TNF group; this was probably not statistically significant due to the sample size.

A Study of Carotid Atherosclerosis in Patients with Non-alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease shares many features of metabolic syndrome and its presence could signify a substantial cardiovascular risk above and beyond that conferred by individual risk factors. This study is an attempt to investigate the association of non-alcoholic fatty liver disease with carotid intima-media thickness and plaque as surrogate measures of increased cardiovascular risk. The study was conducted on 645 non diabetic, non alcoholic subjects in the age range of 20-60years. Metabolic syndrome was assessed by using ATP III and ADA (2005) criteria. Anthropometric factors-waist circumference and blood pressure were measured. Fasting serum samples were analyzed for glucose, triglyceride, cholesterol and its fractions, insulin, alanine and aspartate transaminases, gamma glutamyl transferase and free fatty acids. Insulin resistance and secretion were calculated by homeostasis model and insulin sensitivity by QUICKI index. Liver ultrasonographic scanning was used for assessing fatty liver. Carotid atherosclerosis was assessed by B-mode ultrasonography of common carotid artery and internal carotid artery. The prevalence of non-alcoholic fatty liver disease was 15.6% in non alcoholic population and 68.5% of non-alcoholic fatty liver disease had metabolic syndrome, which was associated with hyperinsulinemia, insulin resistance, insulin insensitivity along with elevated levels of waist circumference, blood pressure, triglyceride, FFA and decreased HDL cholesterol. NAFLD patients had markedly greater carotid intima media thickness than non NAFLD subjects with MCIMT of 591.6±108 and 489.5±132.4μm (P<0.001) and plaque prevalence of 19.2 and 2.2%, respectively, thus the carotid intima media thickness is associated with NAFLD.

Leucocytosis in women with polycystic ovary syndrome (PCOS) is incompletely explained by obesity and insulin resistance

Low-grade chronic inflammation predicts cardiovascular outcomes and is observed in women with polycystic ovary syndrome (PCOS). Whether this is entirely a cause or consequence of insulin resistance (IR) is unknown. Seventy pairs of women with and without PCOS, matched for age, body mass index (BMI) and IR (HOMA, QUICKI and Avignon index), were generated from a larger cohort of 103 women with and 104 BMI-matched women without PCOS. Women with PCOS were studied in the follicular phase of the menstrual cycle. White cell count (WCC), high-sensitivity CRP (hsCRP) and a series of 12 cytokines and growth factors were measured. These inflammatory markers were also compared between women with PCOS and 10 normal women studied in the follicular, peri-ovulatory and luteal stages. When all subjects were compared, WCC (6.75 × 10(9) vs 5.60 × 10(9 ) g/l, P < 0.005), hsCRP (4.04 vs 2.90 mg/l, P < 0.05) and IL-6 (1.11 vs 0.72 pg/ml, P < 0.05) were greater in women with PCOS. Pair-matching for IR eliminated between-group differences in hsCRP and cytokines but did not alter the difference in WCC (6.60 × 10(9) vs 5.60 × 10(9 ) g/l, P < 0.005). WCC was greater in PCOS compared to normal women at all stages of the menstrual cycle. Low-grade inflammation occurs in PCOS. Increased hsCRP and cytokines are associated with IR, but increased WCC is observed even when IR is accounted for. The explanation for this and its clinical significance is unknown.

Lipodystrophy defined by Fat Mass Ratio in HIV-infected patients is associated with a high prevalence of glucose disturbances and insulin resistance

IntroductionCombined antiretroviral therapy (cART) in the treatment of HIV-1 infection has been associated with complications, including lipodystrophy, hyperlipidaemia, insulin resistance (IR) and diabetes.AimsTo compare the prevalence of glucose homeostasis disturbances and IR in HIV patients on cART according to the presence of lipodystrophy (defined clinically and by Fat Mass Ratio) and different patterns of fat distribution and to establish their associations.DesignCross-sectional cohort study.MethodsWe evaluated body composition and IR and insulin sensitivity indexes in 345 HIV-infected adults.ResultsPatients with clinical lipodystrophy (CL) had higher plasma glucose levels than patients without CL, without significant differences in plasma insulin levels, A1c, HOMA-IR, HOMA-B, QUICKI, or MATSUDA index. Patients with lipodystrophy defined by FMR had higher plasma glucose and insulin levels, A1c, HOMA-IR, QUICKI and MATSUDA than patients without lipodystrophy, without differences in HOMA-B. Higher insulin resistance (HOMA-IR ≥ 4) was present in patients with FMR-defined lipodystrophy. Patients with FMR-defined lipodystrophy had a higher prevalence of IFG, IGT and DM than patients without lipodystrophy. Significant associations between HOMA-IR and total, central and central/peripheral fat evaluated by CT at abdominal level were found and no association between HOMA-IR and peripheral fat. Association between HOMA-IR and total and trunk fat but no association with leg and arm fat (evaluated by DXA) was found.ConclusionsIR and glucose disturbances were significantly increased in patients with FMR-defined lipodystrophy. FMR lipodystrophy definition seems to be a more sensitive determinant of insulin resistance and glucose disturbances than clinical definition.