Early unhealthy eating habits underlie morpho-functional changes in the liver and adipose tissue in male rats.
Sofia NogueiraFernanda GarcezSusana SáLuís C MoutinhoArmando CardosoRaquel SoaresBruno M FonsecaSandra LealPublished in: Histochemistry and cell biology (2022)
Early-life consumption of high-fat and sugar-rich foods is recognized as a major contributor for the onset of metabolic dysfunction and its related disorders, including diabetes and nonalcoholic fatty liver disease. The lifelong impact of early unhealthy eating habits that start at younger ages remains unclear. Therefore, to better understand the effects of diet, it is essential to evaluate the structural and functional changes induced in metabolic organs and potential mechanisms underlying those changes. To investigate the long-term effects of eating habits, young male rats were exposed to high-sugar and high-energy diets. After 14 weeks, body composition was assessed, and histopathological changes were analyzed in the liver and adipose tissue. Serum biochemical parameters were also determined. Expression of inflammatory markers in the liver was evaluated by immunohistochemistry. Our results revealed that serum levels of glucose, creatinine, aspartate transaminase (AST), alanine transaminase (ALT), and lipid profile were increased in rats red high-sugar and high-energy diets. Histopathological alterations were observed, including abnormal hepatocyte organization and lipid droplet accumulation in the liver, and abnormal structure of adipocytes. In both unhealthy diet groups, hepatic expression of Toll-like receptor 4 (TLR4), cyclooxygenase 2 (COX-2), and E-selectin were increased, as well as a biomarker of oxidative stress. Together, our data demonstrated that unhealthy diets induced functional and structural changes in the metabolic organs, suggesting that proinflammatory and oxidative stress mechanisms trigger the hepatic alterations and metabolic dysfunction.
Keyphrases
- weight loss
- toll like receptor
- oxidative stress
- adipose tissue
- body composition
- diabetic rats
- physical activity
- early life
- poor prognosis
- inflammatory response
- immune response
- nuclear factor
- glycemic control
- type diabetes
- resistance training
- high glucose
- insulin resistance
- dna damage
- high fat diet
- bone mineral density
- cardiovascular disease
- drug induced
- ischemia reperfusion injury
- high throughput
- metabolic syndrome
- uric acid
- binding protein
- single cell
- electronic health record
- induced apoptosis
- nitric oxide
- nitric oxide synthase
- liver injury
- long non coding rna
- big data
- postmenopausal women
- blood pressure
- high intensity
- preterm birth
- heat shock
- heat stress