Osoczowe stężenia frakcji adiponektyny u kobiet z chorobą Alzheimera

ABSTRACT Introduction Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disease. Typical features of AD include memory loss, social dysfunction and physical impairment. Although the pathological findings in the central nervous system are well established, the etiological factors are poorly known. Recent studies suggested the role of metabolic disturbances in the development of AD neurodegeneration. Adiponectin, an anti-inflammatory and metabolism regulating factor, was linked to AD. Aim The aim was to examine whether adiponectin fractions combined with insulin/insulin resistance-associated metabolic parameters correlate with AD progression. Material and methods The study comprised 98 women: 27 with moderate to severe AD, 31 with AD at early stage and 40 healthy controls, matched for age and BMI. To evaluate memory impairment, the MMSE was performed. Plasma total adiponectin and its high-, medium- and low molecular weights were measured with ELISA. Anthropometric, clinical and metabolic parameters were assessed. Correlations between adiponectin array and measured parameters were evaluated. Results In comparison to the controls, enhanced levels of total and medium molecular weight adiponectin characterized AD individuals. In AD, we found correlations between adiponectin array, and anthropometric and biochemical parameters. After adjustment to BMI, a significant increase of the total adiponectin and high- and medium molecular weight fractions was observed. A negative correlation between low molecular weight adiponectin and MMSE was found. Conclusions Our results indicate a possible link between adiponectin variations and AD. We hypothesize that changes in adiponectin profile observed in AD result from compensatory mechanism against neuropathological processes, as well as from adiponectin homeostasis impairment.Introduction: Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disease. Typical features of AD include memory loss, social dysfunction, and physical impairment. Although the pathological findings in the central nervous system are well established, the aetiological factors are poorly known. Recent studies suggested the role of metabolic disturbances in the development of AD neuro­degeneration. Adiponectin, an anti-inflammatory and metabolism regulating factor, was linked to AD. The aim was to examine whether adiponectin fractions combined with insulin/insulin resistance-associated metabolic parameters cor­relate with AD progression. Material and methods: The study comprised 98 women: 27 with moderate to severe AD, 31 with AD at early stage, and 40 healthy con­trols, matched for age and BMI. To evaluate memory impairment, the Mini-Mental State Examination (MMSE) was performed. Plasma total adiponectin and its high, medium, and low molecular weights were measured with ELISA. Anthropometric, clinical, and metabolic parameters were assessed. Correlations between adiponectin array and measured parameters were evaluated. Results: In comparison to the controls, enhanced levels of total and medium molecular weight adiponectin characterised AD individu­als. In AD, we found correlations between adiponectin array, and anthropometric and biochemical parameters. After adjustment to BMI, a significant increase of the total adiponectin and high and medium molecular weight fractions was observed. A negative correlation between low molecular weight adiponectin and MMSE was found. Conclusions: Our results indicate a possible link between adiponectin variations and AD. We hypothesise that changes in adiponectin profile observed in AD result from compensatory mechanisms against neuropathological processes, as well as from adiponectin homeo­stasis impairment

Total and high molecular weight adiponectin levels in the rat model of post-myocardial infarction heart failure.

Adiponectin is a protein secreted primarily by adipose tissue. It has been suggested that adiponectin plays a protective role in the early phase following myocardial infarction. Our primary aim was to investigate the effects of post-myocardial infarction heart failure well-characterized by left ventricular hemodynamic parameters on the total and high molecular weight adiponectin concentrations in plasma, fat and cardiac tissue. Eight weeks after myocardial infarction or sham operation, total and high molecular weight adiponectin concentrations in plasma, fat, and cardiac tissues were assayed in rats. In addition, hemodynamic parameters and expression of the genes encoding atrial natriuretic peptide and brain natriuretic peptide in left ventricle were evaluated. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels in left ventricle tissue were higher in rats with myocardial infarction-induced heart failure compared with the controls. Similarly, total adiponectin concentration was increased in left ventricle (but not in right ventricle) in rats with postmyocardial infarction heart failure. In contrast, adiponectin levels in plasma and cardiac adipose tissue in rats with postmyocardial infarction heart failure were lower than in sham-operated animals. Furthermore, there were no significant differences in levels of high molecular weight adiponectin in plasma, cardiac tissue or adipose tissue between these two groups. We conclude that in the rat model of post-myocardial infarction heart failure, adiponectin level is increased in left ventricle tissue. This is accompanied by decreased adiponectin levels in plasma and cardiac adipose tissue