Govt Exams
Excessive dietary saturated fat increases liver production of VLDL, which carries triglycerides and cholesterol. VLDL is converted to LDL in circulation, raising LDL levels.
Phospholipids have a glycerol backbone with two fatty acids and a phosphate group, making them amphipathic. This structure is crucial for membrane formation.
HMG-CoA reductase catalyzes the conversion of HMG-CoA to mevalonate, the rate-limiting and key regulatory step in cholesterol biosynthesis. It is targeted by statin drugs.
Familial hypercholesterolemia is caused by mutations in the LDL receptor gene, preventing cells from taking up LDL particles, resulting in elevated blood cholesterol levels.
High cholesterol, particularly LDL cholesterol, can accumulate in artery walls forming atherosclerotic plaques, leading to arterial narrowing (atherosclerosis) and increased risk of heart disease.
Beta-oxidation is the catabolic pathway that breaks down fatty acids in the mitochondria, producing acetyl-CoA which enters the Krebs cycle for ATP production.
Type 2 diabetes shows hepatic insulin resistance leading to impaired glycogenesis (reduced glycogen synthesis) and uncontrolled gluconeogenesis (excessive glucose production). This causes elevated fasting glucose despite normal HbA1c if glycemic control improves later. The liver fails to suppress glucose production in response to insulin.
After 8-12 hours of fasting, hepatic glycogen depletes. The liver then relies on gluconeogenesis from Cori cycle lactate and amino acids to maintain blood glucose.
Glucagon and epinephrine activate phosphorylation cascades that activate glycogen phosphorylase and inactivate glycogen synthase, promoting glycogenolysis.
Haworth projection depicts the cyclic hemiacetal structure of glucose in its pyranose form, clearly showing the anomeric carbon and ring geometry.