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+/-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 (CAD+, n=50) and CAD negative (CAD-, n=58).
Measurement: Assessment of adiponectin isoforms along with metabolic, lipid, and inflammatory profiles.
Results: CAD+ subjects had significantly higher levels of total adiponectin (Tot-Ad) and low-molecular-weight adiponectin (LMW-Ad) than CAD- subjects (P=.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)=0.25, P=.05). This association was not confirmed when CAD+ subjects were analyzed alone. A positive association was found in CAD+ subjects between brain natriuretic peptide (BNP), high-molecular-weight adiponectin (HMW-Ad), and Tot-Ad (r=0.798 and r=0.795, P<.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.
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http://dx.doi.org/10.1111/j.1532-5415.2010.02773.x | DOI Listing |
Aging Cell
October 2024
State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China.
Adiponectin receptor signaling represents a promising therapeutic target for age-related conditions such as osteoporosis and diabetes. However, the literature presents conflicting evidence regarding the role of adiponectin signaling in bone homeostasis and fracture repair across different health states, ages, and disease conditions. These inconsistencies may arise from the complex endocrine and paracrine feedback mechanisms regulating adiponectin, as well as the variability in adiponectin isoforms and receptor expressions.
View Article and Find Full Text PDFPsychoneuroendocrinology
December 2024
Department of Internal Medicine, Endocrine Section, Amsterdam UMC, De Boelelaan 1117, Amsterdam 1081 HV, the Netherlands; Department of Clinical Neuropsychology, Faculty of Behavioral and Movement Sciences, Vrije Universiteit Amsterdam, van der Boechorstraat 7, Amsterdam 1081 BT, the Netherlands. Electronic address:
Background: Leptin and ghrelin have been linked to depressive symptoms in older adults. There is a large overlap between depression and anxiety in this group. It is unclear whether the same associations exist with anxiety.
View Article and Find Full Text PDFSci Rep
August 2024
Department of Internal Medicine I, Division of Cardiology, University Hospital Jena, Friedrich Schiller University, Am Klinikum 1, 07747, Jena, Germany.
Patient age is critical for mesenchymal stem cell quality and differentiation capacity. We demonstrate that proliferation and adipogenic capacity of subcutaneous adipose stem cells (ASCs) from female patients declined with advanced age, associated with reduction in cell nucleus size, increase in nuclear lamina protein lamin B1/B2, and lamin A, upregulation of senescence marker p16INK4a and senescence-associated β-galactosidase activity. Adipogenic induction resulted in differentiation of adipocytes and upregulation of adipogenic genes CCAAT enhancer binding protein alpha, fatty acid binding protein 4, lipoprotein lipase, and peroxisome proliferator-activated receptor-γ, which was not affected by the Sirt-1 activator YK-3-237 or the Sirt-1 inhibitor EX-527.
View Article and Find Full Text PDFBiomedicines
June 2024
School of Kinesiology and Health Science, Muscle Health Research Centre, York University, Toronto, ON M3J 1P3, Canada.
Duchenne muscular dystrophy (DMD) is caused by genetic mutations in the cytoskeletal-sarcolemmal anchor protein dystrophin. Repeated cycles of sarcolemmal tearing and repair lead to a variety of secondary cellular and physiological stressors that are thought to contribute to weakness, atrophy, and fibrosis. Collectively, these stressors can contribute to a pro-inflammatory milieu in locomotor, cardiac, and respiratory muscles.
View Article and Find Full Text PDFEur J Pharmacol
September 2024
Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, 201002, India. Electronic address:
Adiponectin plays key roles in energy metabolism and ameliorates inflammation, oxidative stress, and mitochondrial dysfunction via its primary receptors, adiponectin receptors -1 and 2 (AdipoR1 and AdipoR2). Systemic depletion of adiponectin causes various metabolic disorders, including MASLD; however adiponectin supplementation is not yet achievable owing to its large size and oligomerization-associated complexities. Small-molecule AdipoR agonists, thus, may provide viable therapeutic options against metabolic disorders.
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