• acetyl-CoA
• Dairy cattle
• Hepatic Oxididation Theory
• inflammation
• transition period

The transition period is defined as a period from 3 weeks before to 3 weeks after parturition where dairy cows experience sudden changes in metabolic and immune functions. Around parturition dairy cows face a negative energy balance, energy gap between dietary energy intake and energy demand for manteinance and milk production that occurs around calving. Additionally, during this period is common a reduction in Dry Matter Intake (DMI). This phenomenon results in a lipolytic state in dairy cows with the mobilitation of adipose tissue and the rise of Non-Esterified Fatty Acids (NEFA) concentration in boodstream. NEFA are uptaken from liver and cane be oxidized in Ac. CoA, partially oxidized in ketone bodies or re-esterified in triglycerides (TAG).
The reasons why there is a decrease in DMI are not fully understood but according to Hepatic Oxidation Theory (HOT) this reduction is linked with the increase of fuels in liver. Fuels, such as NEFA and propionate, may undergo an hepatic oxidation, producing energy and causing a satiety signals.
The transition period is often associated with an elevated incidence of metabolic and infectious diseases. Numerous studies have shown that metabolic adaptation that occur during this period (e.g., lipid mobilization, enhanced plasma BHBA and NEFA levels, etc.) are accompanied by alterations in inflammatory responses that modify immune function.
The overall goal of the study was to take a closer look at the link between HOT and inflammation, evaluating how high levels of NEFA and LPS can affect β-oxidation and consequently acetyl-CoA production in mouse hepatocytes. As we expected it has been observed a significative increase (p=0,01) in acetyl-CoA production in cells treated with high levels of NEFA. It has been observed a trend for a treatment effect on CPT-I mRNA expression. There was an upregulation in mRNA expression of cells treated with NEFA compared with control. CPT-I is the enzyme responsable for mitochondrial translocation of NEFA therefore this results are consistent with our hypotesis. Higher levels of NEFA in fact require a greater concentration of CPT-I in order to enter into mitochondial membrane. Moreover it’s been observed treatments effect in Haptoglobin mRNA expression. There is an upregulation of mRNA expression in cells treated with higher levels of NEFA compared with control. Haptoglobin is a positive acute phase proteins so this results are consistent with the hypotesis that high level of hepatic NEFA might promote inframmation.