Diet‐induced adiposity alters the serum profile of inflammation in C57BL/6N mice as measured by antibody array

Abstract

Morbid obesity is considered a systemic inflammatory state. The objective of this project was to characterize the adipokine, cytokine and chemokine protein profile in serum from control, lean and obese mice. We hypothesized that chemokines and cytokines are altered by caloric restriction and diet-induced obesity as a function of changes in body composition. Six-week-old female C57BL/6N mice (n = 12 per group) were randomized to one of three diets: control (fed ad libitum); lean (30% calorie-restricted regimen relative to control) and diet-induced obese (DIO; high calorie diet, fed ad libitum). Body weight, body composition and food intake were monitored throughout the study. After 10 weeks on the diets, blood samples were collected, and adipokine/cytokine/chemokine serum profiles were measured by antibody array. Lean mice, relative to the control group, displayed increased concentrations of insulin-like growth factor (IGF) binding protein-3, -5 and -6 and adiponectin and decreased IGF-1. These mice also showed increased concentrations of interleukin (IL)-10, IL-12 p40/p70, eotaxin, monocyte chemoattractant protein-5 and SDF-1. In contrast, DIO mice displayed increased leptin, IL-6 and LPS-induced chemokine and decreased concentrations of all chemokines/cytokines measured relative to control mice. As such, these data indicate that DIO may lead to an inflammatory state characterized as a shift towards a T helper lymphocyte type 1–skewed responsiveness. The demonstration of differential adipokine, cytokine and chemokine protein profile in control, lean and DIO mice may have implications for immune responsiveness and risk of disease.

Insulin resistance and cancer: the role of insulin and IGFs

“…Immune response alterations and carcinogenesis ILP molecules have been reported to play a crucial role in altered inflammatory responses to infectious challenge commonly observed in insulin resistance-related metabolic disorders (Fenton et al 2009, Bitar & Al-Mulla 2012.…”

Obesity-related systemic factors promote an invasive phenotype in prostate cancer cells

“…5,6 Similar to obese men, obese mice fed a high fat diet also results in increased adiposity, circulating growth factors and inflammation when compared with control mice and may contribute to prostate cancer progression. [7][8][9][10] Studies suggest that cancer cells undergo an epithelialmesenchymal-transition (EMT) program at the initiation of invasion, which is a critical process for metastasis. 11,12 Hallmarks of EMT include loss or decreased protein expression of e-cadherin, increased vimentin and deregulation of b-catenin.…”

Increase of NADPH-diaphorase Expression in Hypothalamus of Stat4 Knockout Mice

“…Th1 immune responses are also related to food intake. Furthermore, Fenton et al (2009) reported that Il12 concentration is closely associated with nutritional status in C57BL/6N mice. Reiss et al (1996) also showed that Il12 up-regulates the production of NO in the CNS.…”

“…Interleukin 12 (Il12)-mediated functions are impaired in Stat4 KO mice Thierfelder et al, 1996). Il12 concentration in blood significantly increases in 30% calorie-restricted animal relative to control (Fenton et al, 2009). It is also known that Il12 activates macrophages and up-regulates nitric oxide (NO) production in response to infection (Reiss et al, 1996).…”