Lam et al., (2007) examined major factors that increase metabolic risks by studying brain glucose metabolism. Secretion of VLDL was monitored in order to relate triglyceride-rich lipoprotein levels to metabolic homeostasis. By measuring the effect of glucose and lactate levels on VLDL secretion, brain glucose levels could ultimately play a critical role in better understanding obesity, diabetes, as well as other metabolic syndromes.

The techniques implemented in order to better understand lipid homeostasis:

• Glucose (Figure 10)was infused into the 3rd cerebral ventricle of Sprague-Dawley rats. The glucose concentration was increased by approximately 70%.

Figure 10: Glucose

•L-Lactate (Figure 11), a product of glucose metabolism, was also injected into the 3rd cerebral ventricle. The lactate level was raised to 5 mM.

Figure 11: Lactic Acid

How did the experiment conclusively map the decrease in VLDL secretion?

•An inhibitor of the Lactate Dehydrogenase (LDH) Complex was incorporated to determine whether metabolism of lactate to pyruvate was a required biochemical step.

•ATP-sensitive potassium (KATP) channels (Figure 12) were blocked with glibenclamide. The channels are essential for regulation of blood glucose levels.

Figure 12: Potassium Channel [Sansom, 2001]

•Also, hepatic levels of stearoyl-CoA as well as oleyl-CoA were monitored to relate the metabolism of glucose and lactate back to liver secretion.

•Nuclear Magnetic Resonance (NMR) and fast performance liquid chromatography were utilized in order to properly measure the secreted VLDL particles.