Efeito da obesidade na resposta inflamatória e metabólica de camundongos com alergia alimentar experimental à ovalbumina

• Ano de defesa: 2014
• Autor(a) principal: Leticia Tamie Paiva Yamada
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Obesidade; Alergia Alimentar; Inflamação; Dieta hiperglicídica; Alimentos
• Link de acesso: http://hdl.handle.net/1843/BUOS-AN4GG2

Obesity is a chronic noncommunicable disease that has now reached epidemic rates. The World Health Organization (WHO) estimates that 2.3 million people in the world are overweight and 700 million are obese. Obesity is a risk factor for several diseases including allergies. It is not known which mechanism but one hypothesis is that chronic inflammation predisposes to hypersensitivity reactions. Recent studies have shown that allergy promotes metabolic dysfunction in addition to inflammation of adipose tissue. Allergic mice, despite exhibiting an important reduction in body weight and adiposity, show a higher inflammatory response in the adipose tissue similar to that observed in obese fat tissue. The aim of this study was to evaluate whether the low-grade inflammatory milieu of mild-obese mice fed a high carbohydrate-containing diet interferes with the allergy response induced by ovalbumin (OVA). BALB/c mice were separated in four groups: (i) Control (C), fed chow diet; (Ii) Allergic (A) fed chow diet; (Iii) Obese (HC) fed the high refined carbohydrate-containing diet (HC Diet) and (iv) Allergic Obesity (HCA) fed HC diet. Groups A and HCA were sensitized with ovalbumin (OVA) subcutaneously with a booster dose 14 days after the first immunization. All of the groups received an oral ovalbumin challenge seven days after the booster. The allergic groups showed increased serum levels of total IgE, IgE and IgG1 anti-ovalbumin, a high activity index score (DAI), aversion to OVA and increased intestinal eosinophil infiltration. Interestingly, the non-allergic mild-obese mice also showed aversion to OVA and an increased number of eosinophils in the gut. After allergic challenge, the OVA+ mice fed the chow diet showed weight loss and lower adiposity in several adipose tissue depots. The OVA+ mice fed the HC diet showed a loss of fat mass only one depot (mesenteric adipose tissue). Furthermore, increased levels of TNF-, IL-6 and IL-10 were observed in this tissue. The allergy associated with mild obesity did not significantly change the metabolic parameters. Our data show that mild-obese allergic mice dont present severe pathological features of food allergy than those exhibited by lean allergic mice. Interestingly, mild obesity promoted by HC diet ingestion itself causes important intestinal disorders that appear to modulate the inflammatory response during antigen challenge.