Adiponectin Isoforms in Elderly Patients with or without Coronary Artery Disease

Abstract

OBJECTIVES:To study the distribution of adiponectin isoforms in a group of very old patients. DESIGN: Cross-sectional. SETTING: Geriatric ambulatory clinic of the Department of Medicine at Policlinico ''Tor Vergata.'' PARTICIPANTS: One hundred eight elderly adults (mean age 85.0 AE 3.2) with or without a history of a previous myocardial infarction as proof of established coronary artery disease (CAD) at least 3 months before entry into the study. Accordingly, subjects were divided into CAD positive (CAD1, n 5 50) and CAD negative (CAD À , n 5 58). MEASUREMENT: Assessment of adiponectin isoforms along with metabolic, lipid, and inflammatory profiles. RESULTS: CAD1 subjects had significantly higher levels of total adiponectin (Tot-Ad) and low-molecular-weight adiponectin (LMW-Ad) than CAD À subjects (P 5.008 for both). LMW-Ad and high-sensitivity C-reactive protein were positively correlated, even after adjustment for waist circumference, sex, glomerular filtration rate, and presence of diabetes mellitus (correlation coefficient (r) 5 0.25, P 5.05). This association was not confirmed when CAD1 subjects were analyzed alone. A positive association was found in CAD1 subjects between brain natriuretic peptide (BNP), highmolecular-weight adiponectin (HMW-Ad), and Tot-Ad (r 5 0.798 and r 5 0.795, Po.001 for all) but not LMW-Ad. CONCLUSION: Distribution of adiponectin isoforms differed in populations of elderly subjects according to the presence of coronary atherosclerosis. The data support the hypothesis for a protective role of LMW-Ad during aging, although additional studies are needed to definitively clarify whether LMW-Ad plays a protective role in older people with a history of CAD. J Am Geriatr Soc 58:702-706, 2010.Key words: adiponectin; elderly; coronary heart disease; inflammation A dipose tissue is an active metabolic tissue that secretes multiple hormones and growth factors, known as adipokines.1 Of them, adiponectin plays a major role because of its beneficial effects on glucose and lipid metabolism.2 Low levels of adiponectin are associated with metabolic disease states, in particular with components of metabolic syndrome, such as central obesity, high triglyceride levels, and low highdensity lipoprotein cholesterol (HDL-C) levels.3 Consistent with this, recent data from the Hoorn Study show that high adiponectin levels are associated with a lower risk of type 2 diabetes mellitus (DM2). 4 Moreover, many clinical studies have shown that hypoadiponectinemia is associated with endothelial dysfunction, greater carotid intima-media thickness, and coronary artery disease (CAD). 3,5,6 Consequently, low adiponectin levels can be included among the main factors underlying the link between DM2 and macrovascular disease, although several recent studies on prospective association between adiponectin and cardiovascular disease (CVD) showed controversial results.7-11 A report on the Hoorn Study found that high levels of adiponectin predict mortality in patients with prevalent CVD.12 Therefore, the cardiovascular action p...

Exercise Induced Adipokine Changes and the Metabolic Syndrome

“…The HMW form may be the most biologically active form regulating glucose homeostasis [19, 20]. Although some studies show that the HMW form has a greater association with cardiovascular diseases [21], it has similar utility for the identification of insulin resistance and metabolic disturbances as does total adiponectin [22]. As opposed to other adipocytokines, plasma levels of adiponectin inversely correlates with body mass index (BMI), intra-abdominal fat, and indices of insulin resistance [23].…”

Reciprocal Effects of Systemic Inflammation and Brain Natriuretic Peptide on Adiponectin Biosynthesis in Adipose Tissue of Patients With Ischemic Heart Disease

“…16 In humans, however, atherosclerosis-related lowgrade inflammation has been associated with both increased 17 and decreased 11 plasma adiponectin, while there is also evidence that advanced, chronic inflammation may even increase adiponectin levels. 18,19 These conflicting findings suggest that mechanisms related with the underlying disease state may override the regulatory role of inflammation on adiponectin biosynthesis in advanced CVD states.…”

An Important Question That Needs to Be Proved: Is There Any Relationship between the Epicardial Fat Thickness and the Coronary Artery Complexity in Patients with Acute Non-ST Elevation Myocardial Infarction?

“…It is widely recognized that the accumulation of epicardial fat tissue is strongly related to the development of atherosclerotic CAD (4,17,24,(24)(25)(26)(27)(28). Certain locally secreted bioactive molecules including low-molecular-weight adiponectin, resistin, interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and monocyte chemotactic protein (MCP)-1 may affect the immunologic and inflammatory responses and, therefore, contribute toward the development of CAD (5,(29)(30)(31). Some sources have suggested the possible mechanism of increased EFT in the development and progression of CAD by decreasing the synthesis of anti-inflammatory cytokines (adiponectin and resistin) and increasing the synthesis of inflammatory cytokines (IL-1, IL-6, and TNF-α) (5-8, 13, 16).…”