Unlike in monogastric mammals, absorption of dietary carbohydrates is insignificant by ruminants since they are efficiently digested by the rumen microbes. Therefore, their liver has a greater critical significance in energy metabolism, as virtually all of their physiological glucose requirements rely on hepatic gluconeogenesis. As energy needs peak toward late gestation and early lactation, they often exceed the level consumed in the diet. In such a state of negative energy balance, animals, including human, mobilize fats from adipose tissue to the liver where they can be degraded to provide energy. However, a state of glucose insufficiency limits the liver capacity for complete oxidative breakdown of fatty acid, which thus enhances both their accumulation as fats in the liver and the process of ketogenesis. If prolonged, such physiology may lead to sever metabolic pathology characterized by fatty liver and toxic levels of blood ketone bodies that result in the clinical signs of pregnancy toxemia. For poorly understood reasons, some individuals are more susceptible than others are to such metabolic failure.
Research in the lab involves the application of tools from Biochemistry and Animal Physiology to:
• Develop an approach to quantify liver metabolic performance.
• Monitor metabolic propensity at an early age for breeding toward improved metabolic capacity, and for reducing the prevalence of pregnancy toxemia.
- Postdoctoral position Liver Metabolism & Sheep Physiology
- Postdoctoral position in Biochemistry & Structural Biology of enzymatic triglyceride breakdown.
- M.Sc. and Ph.D. positions in Sheep Metabolism.