RESUMO
Obesity is associated with a low grade inflammation which contributes to the development of insulin resistance and diabetes. The aim of this study was to assess the total saturated (SFAs), monounsaturated (MUFAs) and polyunsaturated fatty acids (PUFAs) in plasma from asymptomatic obese subjects and to determine the arachidonic/eicosapentanoic acid ratio [ARA/EPA] as a marker of inflammation, and its eventual association with ultrasensitive CRP. Fourteen obese (34.4 ± 11.1y.; BMI: 36.0 ± 4,5 kg/m2) and 12 normal-weight (30.6 ± 7.8y.; BMI: 23,6± 2,4 kg/m2) subjects were recruited and their plasma fatty acids were determined by gas chromatography. usCRP was higher in the obese subjects (p=0,01) and correlates with their body fat content. The percentages of SFAs, MUFAs, PUFAs were not affected in the obese subjects but their concentrations were increased, compared with the control group. However, no differences in the long chain PUFAs (DHA and EPA) concentrations or in the plasmatic ARA/EPA ratio were observed in these subjects. These observations do not support a relation between the ARA/EPA ratio and the presence of low grade inflammation evaluated by plasma usCRP in this group of asymptomatic obese subjects.
La obesidad está asociada con una inflamación de bajo grado que contribuye al desarrollo de la insulino-resistencia y de la diabetes. El objetivo de este estudio fue evaluar las concentraciones plasmáticas de ácidos grasos saturados (AGS), monoinsaturados (AGMI) y poliinsaturados (AGPI) en sujetos obesos asintomáticos y determinar el ratio ácido araquidónico/ácido eicosapentanoico [ARA/EPA] como un posible marcador de inflamación, con su eventual asociación con los niveles de proteína C reactiva ultrasensible (PCRus). Se reclutaron 14 sujetos obesos (34,4 ± 11.1 años; índice de masa corporal: 36,0 ± 4,5 kg/m2) y 12 normopeso (30,6 ± 7.8 años; índice de masa corporal: 23,6 ± 2,4 kg/m2); las concentraciones plasmáticas de ácidos grasos fueron determinados por cromatografía de gases. Los niveles de PCRus fueron más elevadas en los sujetos obesos (p=0,01) y correlacionaron con el contenido de grasa corporal. Los porcentajes relativos de AGS, AGMI, AGPI no se vieron afectados en los sujetos obesos, pero sus concentraciones plasmáticas se incrementaron en comparación con el grupo control. Sin embargo, no se observaron diferencias en las concentraciones de PUFAs de cadena larga (DHA, EPA y ARA) ni en el ratio ARA/EPA en los sujetos obesos. Estas observaciones no apoyan el uso del ratio ARA/EPA como un marcador de inflamación de bajo grado evaluada por PCRus en este grupo de sujetos obesos asintomáticos.
Assuntos
Adolescente , Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem , Ácidos Graxos Monoinsaturados/sangue , /sangue , /sangue , Ácidos Graxos Insaturados/sangue , Obesidade/sangue , Índice de Massa Corporal , Biomarcadores/sangue , Estudos de Casos e Controles , Ácidos Docosa-Hexaenoicos/sangue , Ácido Eicosapentaenoico/sangue , Inflamação/sangueRESUMO
Intestinal microbiota (IM) plays a role in the development of obesity and its associated low grade inflammation. Bacterial colonization of the gastrointestinal tract of germ free mice (without microbiota) increases by 60 percent their fat mass, alters their fasting glucose and insulin levels, triples their hepatic triglycerides and induces adipocyte hypertrophy. IM favors fat storage in adipocytes through the inhibition of Fiaf (Fasting Induced Adipocyte Factor), an inhibitor of lipoprotein lipase. Compared with normal weight subjects, the IM from obese exhibits a higher proportion of Firmicutes/Bacteroidetes and is more efficient in extracting energy from foodstuffs. The loss of bodyweight by a hypocaloric diet reverts the proportion of bacteria to that of lean subjects. The intake of a high fat diet also alters the IM, affecting intestinal barrier function and favoring endotoxinemia. These events increase oxidative and pro-inflammatory processes in plasma and peripheral tissues and increment the risk of insulin resistance. Such events are reverted by the administration of pre-biotics which stimulate the growth of Bifdobacterium and Lactobacillus species in the colon, reestablishing the gut homeostasis. Interestingly, products resulting from the fermentation of prebiotics stimulate the differentiation of enteroendocrine cells and the release of glucagon like peptide 1 and peptide YY, that have insulin like and anorexigenic activities, thus contributing to body weight equilibrium.