Depot specificities of PPARγ ligand actions on lipid and glucose metabolism and their implication in PPARγ-mediated body fat redistribution

2009 ◽  
Vol 4 (5) ◽  
pp. 633-642 ◽  
Author(s):  
William T Festuccia ◽  
Yves Deshaies
Diabetes ◽  
1992 ◽  
Vol 41 (9) ◽  
pp. 1151-1159 ◽  
Author(s):  
E. Bonora ◽  
S. Del Prato ◽  
R. C. Bonadonna ◽  
G. Gulli ◽  
A. Solini ◽  
...  

2005 ◽  
Vol 82 (3) ◽  
pp. 547-552 ◽  
Author(s):  
Nadine R Sahyoun ◽  
Amy L Anderson ◽  
Alka M Kanaya ◽  
Pauline Koh-Banerjee ◽  
Stephen B Kritchevsky ◽  
...  

1999 ◽  
Vol 51 (2) ◽  
pp. 223-230 ◽  
Author(s):  
Eric Renard ◽  
Jacqueline Fabre ◽  
Françoise Paris ◽  
Jacques Reynes ◽  
Jacques Bringer
Keyword(s):  
Body Fat ◽  

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Kochakorn Sithinamsuwan ◽  
Pat Mahachoklertwattana ◽  
Somboon Wankanit ◽  
Suwannee Chanprasertyothin ◽  
Sarunyu Pongratanakul ◽  
...  

Objective. Kisspeptin, a puberty control neuropeptide, has been discovered to have an additional role in metabolism and glucose homeostasis regulation. This study aimed to determine the association of serum kisspeptin with metabolic parameters and glucose metabolism in obese children. Design, Patients and Measurements. A cross-sectional study of 270 obese children was conducted. All children underwent an oral glucose tolerance test and had serum kisspeptin, glycated hemoglobin (HbA1c), and lipid profile measurements. Body fat mass was assessed by bioelectrical impedance analysis. Serum kisspeptin levels of both prepubertal and pubertal children with two HbA1c ranges, <5.7% (normal range) and 5.7–6.4% (prediabetes range), were analyzed and correlated with metabolic parameters and glucose metabolism status. Results. The median (IQR) serum kisspeptin level of only pubertal (not prepubertal) children with prediabetes HbA1c was higher than those with normal HbA1c (53.2 (33.9, 69.8) and 37.8 (29.6, 67.5) pg/mL; p = 0.015 , respectively). There were no differences in serum kisspeptin levels among children with different glucose metabolism status. During pubertal progression, serum kisspeptin reached the highest level at Tanner stage II only in obese boys. Additionally, there was a positive correlation between serum kisspeptin and HbA1c after adjusting for puberty (β = 12.87; p = 0.001 ). No correlations between serum kisspeptin and insulin sensitivity indices, insulin secretion indices, lipid profile, blood glucose, as well as percentage of body fat were demonstrated. Conclusions. Serum kisspeptin levels in pubertal obese children with prediabetes HbA1c were greater than those with normal HbA1c. Serum kisspeptin was positively associated with HbA1c, but not with glucose metabolism status.


2009 ◽  
Vol 297 (5) ◽  
pp. E1097-E1104 ◽  
Author(s):  
Regje M. E. Blümer ◽  
Marc van der Valk ◽  
Mariette Ackermans ◽  
Erik Endert ◽  
Mireille J. Serlie ◽  
...  

HIV-infected patients on antiretroviral therapy frequently develop changes in body fat distribution and disturbances in glucose metabolism, associated with reduced adiponectin levels. Because adiponectin, principally the high-molecular-weight (HMW) form, has insulin-sensitizing properties, we investigated the effects of an increase in adiponectin on glucose metabolism in HIV-lipodystrophy. In this randomized, double-blind, placebo-controlled trial, we included HIV-1-infected patients with severe lipoatrophy, with an undetectable viral load and who had received neither protease inhibitors nor stavudine for ≥6 mo. Patients were randomized to rosiglitazone [8 mg daily ( n = 8)] to increase adiponectin levels or placebo ( n = 5) for 16 wk. Peripheral glucose disposal, glucose production, and lipolysis were measured after an overnight fast and during a hyperinsulinemic-euglycemic clamp using stable isotopes. Body composition was assessed by computed tomography and dual-energy X-ray absorptiometry. Although body fat distribution was unaffected, rosiglitazone increased total plasma adiponectin levels by 107% ( P < 0.02) and the ratio of HMW to total adiponectin by 73% ( P < 0.001). In the placebo group, neither total adiponectin levels ( P = 0.62) nor the ratio of HMW to total adiponectin changed ( P = 0.94). The marked increase in adiponectin induced by rosiglitazone was not associated with significant changes in basal endogenous glucose production ( P = 0.90), basal lipolysis ( P = 0.90), insulin-mediated suppression of glucose production ( P = 0.17) and lipolysis ( P = 0.54) nor with changes in peripheral glucose disposal ( P = 0.13). Acknowledging the limited statistical power of our small study, these findings, if confirmed by larger studies, could question the importance of adiponectin in regulating glucose metabolism in HIV-lipodystrophy.


2011 ◽  
Vol 27 (10) ◽  
pp. 1061-1065 ◽  
Author(s):  
Elena Ferrer ◽  
Luis del Rio ◽  
Esteban Martínez ◽  
Jordi Curto ◽  
Pere Domingo ◽  
...  
Keyword(s):  
Body Fat ◽  

1988 ◽  
Vol 67 (4) ◽  
pp. 760-767 ◽  
Author(s):  
ALAN N. PEIRIS ◽  
MARK F. STRUVE ◽  
ROBERT A. MUELLER ◽  
MARTHA B. LEE ◽  
AHMED H. KISSEBAH

Author(s):  
Gertraud Maskarinec ◽  
Phyllis Raquinio ◽  
Bruce S. Kristal ◽  
Adrian A. Franke ◽  
Steven D. Buchthal ◽  
...  

2018 ◽  
Vol 5 (suppl_1) ◽  
pp. S33-S34 ◽  
Author(s):  
Philip Lackey ◽  
Laurence Brunet ◽  
Jennifer Fusco ◽  
Vani Vannappagari ◽  
Leigh Ragone ◽  
...  

Abstract Background Dolutegravir (DTG), elvitegravir (EVG), raltegravir (RAL), and darunavir (DRV) are commonly used for the treatment of HIV. We assessed the frequency of 6 select disorders after prescription of DTG-, EVG-, RAL-, or DRV-based regimens. Methods HIV-positive patients in the OPERA® Observational Database initiating DTG-, EVG-, RAL-, or DRV-containing regimens were included. Disorders of interest were body fat redistribution/accumulation, pancreatic disorders, and musculoskeletal disorders, as defined in Figures 2–3, as well as immune reconstitution inflammatory syndrome (IRIS), severe systemic rash and hypersensitivity reaction (HSR). Baseline patient characteristics and disorder history were described. The proportion of patients with disorders of interest during follow-up were compared between core agents for each disorder. All events occurring during follow-up were considered prevalent, while incident disorders excluded patients with any history of disorder. To account for multiple comparisons, the Sidak Correction was applied (adjusted α level: 0.017). Results Out of 22,674 patients, 7,860 (35%) initiated DTG, 9,738 (43%) EVG, 1,600 (7%) RAL, and 3,477 (15%) DRV. Baseline demographic and clinical characteristics varied by core agent initiated (Figure 1). Compared with DTG, history of body fat redistribution/accumulation was less frequent in patients initiating EVG, and more frequent in patients initiating RAL (Figure 2). EVG users also had a lower prevalence during follow-up than DTG users (Figure 3). However, there was no difference in new onset of body fat redistribution/accumulation between groups (Figure 3). No difference in prevalent or incident pancreatic or musculoskeletal disorders was detected between core agents (Figure 3). IRIS, severe systemic rash, and HSR occurred in no more than 2 patients per core agent group, with no difference detected between groups. Conclusion Incident body fat redistribution/accumulation, pancreatic disorders, musculoskeletal disorders, IRIS, severe systemic rash, and HSR were rare in this large cohort of patients initiating DTG, EVG, RAL, or DRV. Despite some channeling of patients with a disorder history towards DTG and RAL use, the likelihood of new events did not differ by core agent. Disclosures L. Brunet, Epividian, Inc.: Employee, Salary. ViiV Healthcare: ViiV Healthcare has contracted research with my employer, Epividian, Inc., Employer received funding for research. Merck: Merck has contracted research with my employer, Epividian, Inc., Employer received funding for other research. J. Fusco, Epividian, Inc.: Employee, Salary. ViiV Healthcare: Viiv Healthcare contracted research with my employer, Epividian, Inc., Employer received funding for research. Merck & Co.: Merck contracted research with my employer, Epividian, Inc., Employer received funding for research. V. Vannappagari, ViiV HealthCare: Employee, GlaxoSmithKline Company Stock and Salary. L. Ragone, ViiV Healthcare: Employee and Shareholder, restricted shares and Salary. G. Fusco, Epividian, Inc.: Employee, Salary. ViiV Healthcare: Viiv Healthcare contracted research with my employer, Epividian, Inc., Employer received funding for research. Merck & Co.: Merck contracted research with my employer, Epividian, Inc., Employer received funding for research.


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