The provided source explores the physiological relationship between insulin resistance and dyslipidemia, focusing on how specific enzymes disrupt blood lipid levels. It explains that this condition arises from a functional imbalance between two key lipases responsible for processing fats. Specifically, a reduction in lipoprotein lipase activity prevents the body from clearing triglycerides, causing them to accumulate in the bloodstream. Simultaneously, an increase in hormone-sensitive lipase triggers the excessive release of stored fatty acids from fat cells into the plasma. Together, these enzymatic shifts produce the elevated fat concentrations typically observed in metabolic disorders. This overview highlights the underlying biochemical mechanisms that drive lipid imbalances in insulin-resistant individuals.

Stage I of catabolism involves the breakdown of complex carbohydrates, proteins and lipids into their building block components. This is simply digestion of nutrients which occurs in the intestinal lumen by the action of specific enzymes secreted by the pancreas.

This podcast explains how the body maintains stable blood glucose levels while following a carbohydrate-free ketogenic diet. Since the metabolism of fatty acids produces acetyl-CoA, which cannot be converted into glucose, the body must rely on other mechanisms to fuel the brain and red blood cells. Hormones like glucagon and epinephrine trigger the liver to activate gluconeogenesis, a process that synthesizes new sugar. Because fats are ineligible for this conversion, the liver utilizes the carbon skeletons of amino acids derived from dietary protein to create glucose. Ultimately, the high protein content of a keto diet is essential for replenishing glycogen stores and ensuring the body has a consistent energy supply.