Immune responsiveness in a rat model for type II diabetes (Zucker rat, fa/fa): susceptibility to Candida albicans infection and leucocyte function

Plotkin, Balbina J.; Paulson, Dennis J.; Chelich, A.M.; Jurak, D.; Cole, Jennifer E.; Kasimos, John N.; Burdick, John M.; Casteel, Nancy

doi:10.1099/00222615-44-4-277

Cited by 68 publications

(36 citation statements)

References 28 publications

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“…Furthermore, the UCP2 gene plays a role in the regulation of the inflammatory response. Increased UCP2 mRNA expression is related with a decreased oxidative burst activity of phagocytic cells (1,17), which is in agreement with previously reported data (13) showing that cafeteria-fed rats had a poor oxidative burst activity. Trecadrine treatment seemed not to restore UCP2 mRNA expression to normal levels, which contributes to understand the obtained data.…”

Section: Discussionsupporting

confidence: 82%

Effects of a β3-adrenergic agonist on the immune response in diet-induced (cafeteria) obese animals

Lamas

Martínez

Marti

2003

J. Physiol. Biochem.

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Molecules with affinity for beta3-adrenoceptors are not only effective anti-obesity agents in rodent models, but may play a role in the regulation of the immune response. The aim of the current investigation was to analyse the effects of trecadrine on the immune response in diet-induced (cafeteria) obese rats. Male Wistar rats were divided into 2 groups, the control group (C, n=9) was fed with the standard pelleted chow laboratory diet, while the other group was fed with a high-fat (cafeteria) diet. Cafeteria-fed rats were divided into two new subgroups (n=9 each), which received either i.p. saline (obese, O) or trecadrine (1mg/kg/day) (obese+trecadrine, O+T) daily for 5 weeks. Lymphocyte subpopulations and the proliferative response were determined by validated procedures. The administration of trecadrine was able to prevent the onset of obesity in cafeteria-fed rats. Trecadrine-treatment to obese animals appeared to improve the number of lymphocyte subpopulations (CD4+ and CD8+) as compared to those animals only receiving the high-fat diet, being the values of the trecadrine-treated animals on the high-fat diet similar to the control rats. However, the lymphoproliferative response when stimulated with several mitogens was markedly reduced by the cafeteria intake and was further decreased by the beta3-adrenergic administration. The spleen mRNA expression level of UCP2, PPARgamma and Ob-Rb were not affected by the trecadrine treatment. Summing up, at the immune system level, trecadrine administration increased the proportion of CD4+ spleen lymphocytes, although it was not able to restore the lymphocyte proliferative response which was depressed.

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Section: Discussionsupporting

confidence: 82%

Effects of a β3-adrenergic agonist on the immune response in diet-induced (cafeteria) obese animals

Lamas

Martínez

Marti

2003

J. Physiol. Biochem.

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“…A negative correlation exists between UCP 2 gene expression in macrophages and ROS production. Furthermore, energy restriction has been found to decrease free radical production in mitochondria [24,52]. In this context, higher levels of UCP 2 in spleen may contribute to a poor innate immune response.…”

Section: Discussionmentioning

confidence: 95%

Energy restriction restores the impaired immune response in overweight (cafeteria) rats

Lamas

Martínez

Marti

2004

The Journal of Nutritional Biochemistry

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“…In obese Zucker rats, NK cell activity has been reported to be suppressed, and the effect found to be reversible through exercise training via improved lymphocyte glucose uptake and enhanced GLUT-1 expression. On the other hand, phagocytosis was not affected by obesity, but obese Zucker rats had diminished ability to kill phagocytosed bacteria as compared to control rats due to lower oxidative burst activity (Plotkin et al, 1996).…”

Section: Obesity and Immunocompetence O Lamas Et Almentioning

confidence: 98%

Obesity and immunocompetence

2002

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The increasing worldwide prevalence of obesity is a major health problem since excessive body weight constitutes a risk factor in a number of chronic diseases. It has been reported that obese individuals are more susceptible to infection than lean subjects; however, the underlying factors are not fully understood. Limited and often controversial information exists comparing immunocompetence in obese and nonobese subjects as well as the cellular and molecular mechanisms involved, although much evidence supports a link between adipose tissue metabolism and immunocompetent cell functions. The complexity and heterogeneity of nutritional status and immune system interactions require an integral study of the immunocompetent cells, their subsets and products, as well as specific and non-specific inducer=regulatory systems in situations of human obesity. Additional research is needed to determine the clinical implications of these alterations on immunity and whether various interventions such as weight loss, exercise or nutrient supplementation could help to ameliorate them.

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Immune responsiveness in a rat model for type II diabetes (Zucker rat, fa/fa): susceptibility to Candida albicans infection and leucocyte function

Cited by 68 publications

References 28 publications

Effects of a β3-adrenergic agonist on the immune response in diet-induced (cafeteria) obese animals

Effects of a β3-adrenergic agonist on the immune response in diet-induced (cafeteria) obese animals

Energy restriction restores the impaired immune response in overweight (cafeteria) rats

Obesity and immunocompetence

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