Diet-induced Obesity Differentially Modulates Cardiac Inflammatory Status in the C57 and FVB Mouse Strains.

BACKGROUND: Cardiovascular diseases correspond to the highest risk of sudden death worldwide, and obesity is largely related to be an increased risk factor. There is a higher prevalence of arterial hypertension in obese individuals, including the presence of cardiac hypertrophy. It is already known the role of toll-like receptors [TLR], mainly 2 and 4 in heart cells, as fundamental to the process of cardiac hypertrophy. Obesity has been studied as an activator of damage-associated molecular patterns [DAMPs], which use the TLR signaling pathway to increase the nuclear factor of inflammation, NF-kB, increasing cytokine expression in heart tissue. It's already known that FVB/N and C57BL/6 mouse strains have different behaviors in relation to metabolism, but the difference in cardiac tropism and innate immune system modulation are not clear. METHODS: The present study aimed to evaluate the contribution of innate immune factors to cardiac hypertrophy induced by an experimental model of obesity comparing two mouse strains: C57BL/6 and FVB/N. Both strains were submitted to a high-fat diet containing 23% protein, 35.5% carbohydrate, and 35.9% fat for 68 days. Hearts were collected, weighed, and submitted to RT-qPCR, and the serum was analyzed by Bioplex. RESULTS: We observed an increase in heart mass after 68 days in both strains. This was followed by an increase of α-actin only in C57BL/6 while ANF was increased in FVB/N. Gene expression of innate immune components and inflammatory cytokines were only increased in C57BL/6, but not in FVB/N. CONCLUSION: Based on the results obtained, we verified that C57BL/6 mice had a more robust action of innate immune system then FVB/N.

Is the FVB/N mouse strain truly resistant to diet-induced obesity?

C57Bl/6J mice are the gold standard animal model of diet-induced obesity. These animals become obese with higher adiposity, blood fasting glucose, triglycerides, and total cholesterol when fed a high-fat diet (HFD). Conversely, the FVB/N mouse line is thought to be resistant to diet-induced obesity, with low or no weight gain and adiposity in response to a HFD In this study, we investigated whether FVB/N mice are resistant or susceptible to metabolic disorder that is promoted by a HFD Biometric parameters and blood chemistry were analyzed in C57Bl/6J and FVB/N mice that were fed a chow diet or HFD Glucose and insulin sensitivity were assessed by performing the glucose tolerance test and measuring serum insulin/glucose and homeostasis model assessment-insulin resistance. Metabolism-related gene expression was investigated by real-time reverse transcription polymerase chain reaction. Adipocyte morphology and liver steatosis were evaluated using standard histology. FVB/N mice had higher adiposity than C57Bl/6J mice that were fed a chow diet and were glucose intolerant. FVB/N mice that were fed a HFD presented higher insulin resistance and greater liver steatosis. Epididymal white adipose tissue exhibited severe inflammation in FVB/N mice that were fed a HFD The FVB/N mouse strain is suitable for studies of diet-induced obesity, and the apparent lack of a HFD-induced response may reveal several strain-specific events that are triggered by a HFD Further studies of the FVB/N background may shed light on the complex multifactorial symptoms of obesity and metabolic syndrome.