Serum resistin concentrations are higher in human obesity but independent from insulin resistance.

UNLABELLED: Although obesity may be linked to resistin, the role of resistin in humans is still controversial. Conflicting results of the associations between resistin and BMI and measures of insulin resistance were reported. In view of the yet unexplained role of resistin in human obesity, the aim of this study was to examine correlations between serum resistin concentrations and the degree of human obesity and insulin sensitivity. For this purpose, we investigated 2 homogenous groups of obese and non obese humans, in whom the presence of obesity was the solely differentiating factor. The WHO definition of obesity was used. Study group consisted of 136 obese subjects (75 women and 61 men) and 48 non-obese controls (31 women, 17 men) aged 48.0 ± 10.1, and 48.8 ± 13.4 yrs, respectively. RESULTS: Obese subjects showed higher resistin concentrations than non obese controls (24.89 ± 9.73 ng/mL, median 26.61 vs. 15.34 ± 4.68 ng/mL, median 14.76, P < 0.0001). Resistin concentrations correlated with BMI in the whole cohort (r = 0.4296, P < 0.0001), but not in obese and non-obese subjects separately (r = 0.1418, P = 0.0997; r = 0.2712, P = 0.0623, respectively). Moreover, serum resistin was not influenced by insulin resistance in either group examined. CONCLUSION: Although concentrations of resistin differ between obese and non-obese humans, no relationship between resistin concentration and insulin resistance has been found. Correlations between resistin and BMI are present only in a mixed population but disappear in non obese and obese subjects when analyzed separately.

Leptin, soluble leptin receptors, free leptin index, and their relationship with insulin resistance and BMI: high normal BMI is the threshold for serum leptin increase in humans.

Leptin binds to the soluble form of its receptor (sOB-R). Leptin and sOB-R balance (free leptin index, FLI) reflect leptin activity. Leptin correlates with obesity and insulin resistance, but it remains uncertain whether sOB-R and FLI also do the same. Therefore, the aim of this study was to measure serum leptin, sOB-R, and FLI, and evaluate their associations with BMI and insulin resistance. We studied 145 obese and 49 nonobese humans. Obesity was defined according to WHO (BMI >30 kg/m (2)). Results are given as: median and interquartile range, obese vs. nonobese, respectively. Leptin (ng/ml): 30.83, 37.27 vs. 8.31, 10.04; sOB-R (ng/ml): 17.62, 17.05 vs. 27.25, 11.30; FLI: 231.2, 310.0 vs. 30.85, 27.77; HOMA: 5.99, 6.64 vs. 3.92, 4.52; p<0.001 for all. Serum leptin, sOB-R, and FLI did not correlate with insulin resistance separately in obese and nonobese humans. Leptin and FLI, but not sOB-R, were associated with insulin resistance in obese and nonobese subjects examined together. Leptin, sOB-R and FLI differed between obese and nonobese humans, and, except sOB-R, correlated with BMI. In piecewise linear regression, BMI threshold where leptin increased was 24.6 (r=0.5969, p=0.00016 and <0.00001). Leptin and its free index, but not sOB-R, correlate with BMI only in a mixed obese and nonobese human cohort, and not in isolated obese or nonobese groups. Moreover, BMI threshold where leptin starts to increase is 24.6 kg/m (2), which is lower than the cutoff for overweight. Under the conditions, metabolic abnormalities may occur in parallel to much lower BMI levels as expected so far.

Serum adiponectin concentrations are not related to glycosylated hemoglobin levels (HbA1c) in obese diabetic and non-diabetic caucasians.

UNLABELLED: Although circulating adiponectin has been inversely correlated with obesity, type 2 diabetes and serum glycosylated hemoglobin (HbA1c) in humans, contradictory reports on that subject exist. In this study, serum concentrations of adiponectin in obese non-diabetic and diabetic humans were measured to examine whether they were associated with levels of HbA1c. The WHO definitions of obesity and diabetes were used. One hundred and five obese euglycemic subjects and 49 obese diabetics (aged 51+/-6.9, and 52+/-6.7 years, respectively) were studied. Their BMI, HbA1c and % of body fat were measured. Adiponectin was determined by an enzyme-linked immunosorbent assay. Although the serum adiponectin concentrations differed between diabetics and non-diabetics ( P<0.01), they were not correlated with HbA1c (r=-0.0814; P=0.5823, and r=-0.1861; P=0.1099, for diabetics and non-diabetics, respectively). Both diabetics and non-diabetics were segregated into tertiles according to their HbA1c levels. Plasma adiponectin did not differ significantly between the high (H), intermediate (I), and low (L) HbA1c tertiles. CONCLUSION: Concentrations of adiponectin were not correlated with levels of glycosylated hemoglobin in the diabetic and non-diabetic subjects examined.

The Y111 H (T415C) polymorphism in exon 3 of the gene encoding adiponectin is uncommon in Polish obese patients.

The genetic background of obesity is under research. Obesity-related phenotype candidate genes include the gene encoding adiponectin (AdipoQ). In this study, exon 3 of the adiponectin gene was screened for the Y111 H (Tyr111His, or T415C, rs17366743) polymorphism, and adiponectin serum concentrations were measured in 206 obese subjects (110 women and 96 men, aged 50.5+/-16.9 years). Their BMI, % of body fat, plasma glucose, insulin, and glycosylated hemoglobin were measured. Adiponectin was determined by enzyme-linked immunosorbent assay. Genomic DNA was extracted from peripheral blood leukocytes. A fragment of exon 3 of the adiponectin gene was amplified in PCR and screened for the Y111 H polymorphism in SSCP analysis. Genetic screening revealed a different SSCP pattern in 2 subjects. Subsequent genotyping disclosed the TC genotype in both subjects, resulting in Y111 H heterozygote variant frequency of 0.01 in the whole cohort. Other results for SNP (single nucleotide polymorphism) positive and negative subjects were as follows, respectively: BMI (kg/m (2)) 39.95+/-9.83 vs. 38.12+/-8.56; waist circumference (cm) 122+/-18.4 vs.115+/-16; glucose (mmol/l) 7.51+/-1.86 vs. 5.56+/-0.74; HbA1c (%) 7.55+/-1.86 vs. 6.58+/-1.36; body fat (%) 51+/-2 vs. 44+/-10; plasma insulin (mU/l) 28.92+/-16.50 vs. 37.59+/-47.34; adiponectin (ng/ml) 1301+/-15.8 vs. 5682+/-4156. Due to a proportion of 2 vs. 204, statistical calculations were not possible. The Y111 H adiponectin gene variant is uncommon in Polish obese subjects. Although we observed low adiponectin concentrations in Y111 H SNP heterozygote carriers, this finding was not confirmed by statistics.

Circulating serum adiponectin concentrations do not differ between obese and non-obese caucasians and are unrelated to insulin sensitivity.

Reduced serum levels of adiponectin in obesity and insulin resistance seem paradoxical, since adipose tissue is the only source of adiponectin, and reports on that subject are contradictory. The aim of this study was to investigate the concentrations of adiponectin in non-obese and obese normoglycemic humans, and to determine the correlation between adiponectin and HOMA index of insulin sensitivity. Based on the WHO definition of obesity, 145 obese subjects and 49 non-obese controls (aged 20-55 years) were studied. The serum adiponectin concentrations did not differ between subjects and controls (p=0.6398) and were not correlated with HOMA index (r=-0.0211; p=0.8048, and r=-0.0523; p=0.4757, for subjects and controls, respectively). Adiponectin was not correlated with HOMA index in females (r=-0.0521; p=0.6546, and r=-0.0825; p=0.3981, for female subjects and controls, respectively) as well as in males (r=0.0033; p=0.9791, and r=0.0123; p=0.9131, for male subjects and controls, respectively). These results lead to the conclusion that neither the concentrations of adiponectin differ between obese and non-obese humans, nor does any relationship between adiponectin concentration and insulin sensitivity exist.

Hypothyroidism has no impact on insulin sensitivity assessed with HOMA-IR in totally thyroidectomized patients.

UNLABELLED: The influence of thyroid hormones on insulin and glucose metabolism is controversial. We examined the impact of hypothyroidism on insulin sensitivity in 22 hypothyroid patients (15 females and 7 males, mean age 51.0 +/- 12.36 yrs). All subjects had a history of total thyroidectomy and radioiodine ablation for differentiated thyroid cancer. Each subject ceased levothyroxine treatment six weeks prior to admission. The controls were 17 healthy individuals, 6 women and 11 men, mean age 55.12 +/- 14.17 years. TSH, free thyroxine, and the HOMA index of insulin sensitivity, as well as HOMA B (%) and HOMA S (%) were assessed. Insulin sensitivity was compared between the groups, and the correlation between FT4 and TSH and insulin sensitivity was calculated. RESULTS: The mean FT4 was 4.6 +/- 4.64 pmol/L in the examined group vs. 16.2 +/- 1.8 pmol/L in controls, p<005; TSH 72.11 +/- 36.73 pmol/L vs. 1.24 +/- 1.07 pmol/L, p<0.005; plasma glucose 4.68 +/- 0.47 mmol/L vs. 5.04 +/- 0.62mmol/L, p=0.0436; plasma insulin 8.07 +/- 9.39 microU/mL vs. 7.24 +/- 4.06 microU/mL, p=0.7877; HOMA index 1.79 +/- 2.53 vs. 1.69 +/- 1.09, p=0.5148; HOMA B (%) 102.46 +/- 41.59 vs. 85.95 +/- 26.87, p=0.1926, and HOMA S (%) 150.46 +/- 95.90 vs. 153.80 +/- 108.85, p= 0.6710, in subjects and controls, respectively. The levels of insulin sensitivity did not differ significantly between the two groups. FT4 and TSH did not influence the insulin sensitivity in either group, the correlation was insignificant, respectively p=0.5426 and p=0.8175 in the examined group, and p=0.172 and p=0.4509 in the controls. CONCLUSION: Hypothyroidism has no impact on insulin sensitivity in the examined group.

Prolonged ventricular repolarization measured by corrected QT interval (QTc) in subclinical hyperthyroidism.

UNLABELLED: Overt hyperthyroidism and hypothyroidism exert a major effect on cardiac function and on ECG. The influence of subclinical hyperthyroidism on the circulatory system is still under debate. Few studies examined the effect of thyroid hormones on ventricular repolarization measured by corrected QT interval (QTc). Longer QTc is associated with increased risk of arrhythmia and cardiac mortality. The aim of this study was to examine the influence of subclinical hyperthyroidism on ventricular repolarization measured by corrected QTc in a standard 12-lead electrocardiogram. The examined group consisted of thirty-two patients with subclinical hyperthyroidism; the controls were thirty-nine healthy individuals. In the group with subclinical hyperthyroidism, we observed a significant increase in heart rate (80.3 +/- 10.59 vs. 73.7 +/- 11.37 bpm, p < 0.05). The mean corrected QTc was 0.434 +/- 0.0207 seconds and 0.414 +/- 0.0208 in the examined groups and in controls, respectively (p < 0.001). QTc did not correlate with free thyroxin concentrations (p = 0.5084). CONCLUSION: Corrected QT intervals were significantly longer in patients with subclinical hyperthyroidism.

[Glycemia control in diabetic pregnancies under intensive insulin treatment with and without the aid of the Camit-Diacomp system]. / Kontrola wyrównania glikemii u ciezarnych z cukrzyca leczonych intesywna insulinoterapia przy pomocy oraz bez systemu Camit-Diacomp.

The efficiency of glycemia control was compared in two groups of insulin dependent diabetic pregnancies treated with insulin, with and without the aid of the Camit-Diacomp system. The efficiency of glycemia control was analysed in all three trimesters of pregnancy. Mean diurnal fluctuations of glycemia levels in both study groups were compared. The clinical state of newborns, their glycemia and insulin levels in cord blood were analysed as well. No statistically significant differences of glycemia levels between the two compared groups of patients were found, however the observed significant differences of the HbA1C levels between these groups can speak in favour of the efficiency of treatment under the Camit-Diacomp system, which enables a more precise self control of the treatment and dosage of insulin.