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
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