Javier Gómez-Ambrosi1, Victoria Catalán1, Amaia Rodríguez1, Patricia Andrada2, Beatriz Ramírez1, Patricia Ibáñez3, Neus Vila2, Sonia Romero2, María A Margall2, María J Gil4, Rafael Moncada5, Víctor Valentí6, Camilo Silva3, Javier Salvador3, Gema Frühbeck7. 1. Metabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Pamplona, Spain. 2. Department of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain. 3. Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Pamplona, Spain Department of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain. 4. Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Pamplona, Spain Department of Biochemistry, Clínica Universidad de Navarra, Pamplona, Spain. 5. Department of Anesthesiology, Clínica Universidad de Navarra, Pamplona, Spain. 6. Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Pamplona, Spain Department of Surgery, Clínica Universidad de Navarra, Pamplona, Spain. 7. Metabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Pamplona, Spain Department of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain gfruhbeck@unav.es.
Abstract
OBJECTIVE: It has been suggested that individuals with the condition known as metabolically healthy obesity (MHO) may not have the same increased risk for the development of metabolic abnormalities as their non-metabolically healthy counterparts. However, the validity of this concept has recently been challenged, since it may not translate into lower morbidity and mortality. The aim of the current study was to compare the cardiometabolic/inflammatory profile and the prevalence of impaired glucose tolerance (IGT) and type 2 diabetes (T2D) in patients categorized as having MHO or metabolically abnormal obesity (MAO). RESEARCH DESIGN AND METHODS: We performed a cross-sectional analysis to compare the cardiometabolic/inflammatory profile of 222 MHO and 222 MAO patients (62% women) matched by age, including 255 lean subjects as reference (cohort 1). In a second cohort, we analyzed the adipokine profile and the expression of genes involved in inflammation and extracellular matrix remodeling in visceral adipose tissue (VAT; n = 82) and liver (n = 55). RESULTS: The cardiometabolic and inflammatory profiles (CRP, fibrinogen, uric acid, leukocyte count, and hepatic enzymes) were similarly increased in MHO and MAO in both cohorts. Moreover, above 30%of patients classified as MHO according to fasting plasma glucose exhibited IGT or T2D [corrected]. The profile of classic (leptin, adiponectin, resistin) as well as novel (serum amyloid A and matrix metallopeptidase 9) adipokines was almost identical in MHO and MAO groups in cohort 2. Expression of genes involved in inflammation and tissue remodeling in VAT and liver showed a similar alteration pattern in MHO and MAO individuals. CONCLUSIONS: The current study provides evidence for the existence of a comparable adverse cardiometabolic profile in MHO and MAO patients; thus the MHO concept should be applied with caution. A better identification of the obesity phenotypes and a more precise diagnosis are needed for improving the management of obese individuals.
OBJECTIVE: It has been suggested that individuals with the condition known as metabolically healthy obesity (MHO) may not have the same increased risk for the development of metabolic abnormalities as their non-metabolically healthy counterparts. However, the validity of this concept has recently been challenged, since it may not translate into lower morbidity and mortality. The aim of the current study was to compare the cardiometabolic/inflammatory profile and the prevalence of impaired glucose tolerance (IGT) and type 2 diabetes (T2D) in patients categorized as having MHO or metabolically abnormal obesity (MAO). RESEARCH DESIGN AND METHODS: We performed a cross-sectional analysis to compare the cardiometabolic/inflammatory profile of 222 MHO and 222 MAO patients (62% women) matched by age, including 255 lean subjects as reference (cohort 1). In a second cohort, we analyzed the adipokine profile and the expression of genes involved in inflammation and extracellular matrix remodeling in visceral adipose tissue (VAT; n = 82) and liver (n = 55). RESULTS: The cardiometabolic and inflammatory profiles (CRP, fibrinogen, uric acid, leukocyte count, and hepatic enzymes) were similarly increased in MHO and MAO in both cohorts. Moreover, above 30%of patients classified as MHO according to fasting plasma glucose exhibited IGT or T2D [corrected]. The profile of classic (leptin, adiponectin, resistin) as well as novel (serum amyloid A and matrix metallopeptidase 9) adipokines was almost identical in MHO and MAO groups in cohort 2. Expression of genes involved in inflammation and tissue remodeling in VAT and liver showed a similar alteration pattern in MHO and MAO individuals. CONCLUSIONS: The current study provides evidence for the existence of a comparable adverse cardiometabolic profile in MHO and MAO patients; thus the MHO concept should be applied with caution. A better identification of the obesity phenotypes and a more precise diagnosis are needed for improving the management of obese individuals.
Authors: Ada M Cuevas; Mariana Lazo; Isabel Zuñiga; Fernando Carrasco; Jim J Potter; Veronica Alvarez; Marcos Berry; Fernando Maluenda; Mario Ferrario; Jeanne M Clark Journal: Metab Syndr Relat Disord Date: 2017-01-11 Impact factor: 1.894