Metabolic Changes in Androgen-Deprived Nondiabetic Men With Prostate Cancer Are Not Mediated by Cytokines or aP2
Autor: | Karol M. Pencina, Robert R. Edwards, Zhuoying Li, Thomas G. Travison, Thiago Gagliano-Jucá, M Furkan Burak, Shehzad Basaria |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
Blood Glucose
Male medicine.medical_specialty Antineoplastic Agents Hormonal Endocrinology Diabetes and Metabolism medicine.medical_treatment Lipoproteins Clinical Biochemistry 030204 cardiovascular system & hematology Fatty Acid-Binding Proteins Biochemistry Proinflammatory cytokine Androgen deprivation therapy 03 medical and health sciences Prostate cancer 0302 clinical medicine Endocrinology Insulin resistance Diabetes mellitus Internal medicine medicine Humans Insulin Testosterone Prospective Studies Clinical Research Articles Aged Dyslipidemias Aged 80 and over Anthropometry business.industry Biochemistry (medical) Prostatic Neoplasms Androgen Antagonists Middle Aged medicine.disease Lipids 030220 oncology & carcinogenesis Homeostatic model assessment Cytokines Inflammation Mediators Insulin Resistance business |
Popis: | CONTEXT: Androgen deprivation therapy (ADT) remains the cornerstone of management of prostate cancer (PCa). Previous studies have shown that men undergoing ADT develop insulin resistance and diabetes, but the mechanisms behind ADT-induced metabolic abnormalities remain unclear. OBJECTIVE: To evaluate the role of inflammatory cytokines and adipocyte protein-2 (aP2) in ADT-induced metabolic dysfunction. PARTICIPANTS AND INTERVENTIONS: This 6-month prospective cohort study enrolled nondiabetic men with PCa about to undergo ADT (ADT group) and a control group of nondiabetic men who had previously undergone prostatectomy for localized PCa and were in remission (non-ADT group); all participants had normal testosterone at study entry. Fasting blood samples were collected at baseline and at 6, 12, and 24 weeks after initiation of ADT and at the same intervals in the non-ADT group. Glucose, insulin, lipids, inflammatory cytokines, and C-reactive protein were measured. We also measured serum aP2, an adipocyte-secreted protein that promotes hepatic glucose production. Homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. RESULTS: Seventy-three participants formed the analytical sample (33 ADT, 40 non-ADT). HOMA-IR increased in the ADT group (estimated change = 0.25; P = 0.05), but was unchanged in the non-ADT group (0.11; P = 0.342). Serum concentrations of inflammatory cytokines or aP2 did not change significantly. There was a treatment-associated increase in total (16 mg/dL; P < 0.001), high-density lipoprotein (8 mg/dL; P < 0.001), and low-density lipoprotein (7 mg/dL; P = 0.02) cholesterol. CONCLUSION: ADT-induced metabolic abnormalities were not associated with changes in circulating inflammatory cytokines or aP2 levels. |
Databáze: | OpenAIRE |
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