Date of Award

Spring 5-15-2022

Degree Type

Thesis

Degree Name

Master of Science (MS)

Department

Nutrition Science and Dietetics

Advisor(s)

Ramalingam, Latha

Keywords

fish oil, gene, liver, metabolic health, obesity, paternal obesity

Subject Categories

Food Science | Life Sciences | Nutrition | Physiology

Abstract

Obesity and overweight arise due to an abnormal fat accumulation in the body that presents a risk to health. Individuals with body mass index (BMI) of greater than 30 kg/m2 are considered obese. CDC data show that 43% of the adults in the US are obese. The prevalence of obesity as well as its strong association with cardiovascular and metabolic diseases are the serious concerns of public health which calls for the need of appropriate diet/nutrition that can minimize the negative effect of obesity. Literature suggests that 50% of the contribution to obesity can be attributed to genetics. However, studies are mostly focused on the association between mother's obesity (maternal) and child's health only. Father's obesity (paternal) although equally important, has been scarcely studied. In my research, we focused on the effect of paternal obesity on child's health, and experimentally investigated effects of fish oil (FO) on the obese father that can mitigate risk of obesity and associated diseases on children. Due to several metabolic benefits of FO, we hypothesized that the FO supplementation to an obese father during the pre-conception period could improve metabolic health of the offspring. Three groups of male mice were fed low fat (LF), high fat (HF) or high fat supplemented diet with FO for 10 weeks and then allowed to mate with female mice (all female mice fed with LF only). After the offspring were born, birth weight was recorded weekly. Glucose and insulin tolerance were performed in the offspring at 12 weeks of age. Offspring were sacrificed at 16 weeks of age to collect muscle, liver, and adipose tissue. To comprehend the short-term and long-term effect of the paternal obesity and FO intervention, we investigated offspring sacrificed at 8 weeks of age (short-term) and at 16 weeks of age (long-term). It was observed that the offspring of HF fed fathers were obese, while offspring of FO fed fathers were metabolically healthier during their later stage of life. Glucose and insulin tolerances of offspring of FO fed fathers were significantly improved as compared to offspring of HF fed fathers. Hematoxylin and eosin staining revealed higher deposition of fat in the liver of offspring of HF fed fathers, which was not evident in the offspring of FO fed fathers. Gene expression analyses indicated significantly higher expression of pro-inflammatory biomarkers (IL6, TNF-a, PDK4, SREBP-1c) in the liver of offspring of HF fed fathers as compared to that of offspring of LF fed fathers (n = 8-10, p < 0.05). Further these markers were lower significantly in offspring of FO supplemented father. Similar findings were obtained in the case of the fatty acid synthesis biomarker (FASN) where expression in liver was significantly higher in offspring of HF fed father as compared to offspring of LF fed fathers. This was subsequently minimized due to FO supplementation in obese father. The analysis of fatty acid oxidation biomarkers showed an interesting outcome with higher expression of FOXO and CPT- 1 in liver of offspring of FO fed fathers as compared to that on offspring of HF fed fathers at 8 weeks of age. This differentiation later was diminished with no significant difference observed at 16 weeks of age. Overall, the expression of biomarkers highlighted the role of FO supplementation on paternal obesity to eliminate the risk of metabolic and cardiovascular diseases in offspring. Further probe is necessary to understand the expression and metabolism of fatty acid oxidation biomarkers in paternal obesity. The present study summarizes that FO supplementation in fathers shows potential to reduce metabolic and cardiovascular diseases in children.

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Open Access

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