Govt. Exams
Entrance Exams
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.
NADPH from the oxidative pentose phosphate pathway is essential for reductive biosynthesis of fatty acids and cholesterol, which occur predominantly in the fed state.
HFI results from aldolase B deficiency, preventing cleavage of fructose-1-phosphate into DHAP and glyceraldehyde, leading to accumulation and hepatotoxicity.
Von Gierke disease (GSD Type I) results from glucose-6-phosphatase deficiency, preventing final step of both gluconeogenesis and glycogenolysis, causing severe hypoglycemia.
Liver glycogen maintains blood glucose but cannot directly supply glucose-6-phosphate to other tissues as glucose-6-phosphate cannot cross cell membranes.
Muscle glycogen is the primary energy source during high-intensity exercise because muscle lacks glucose-6-phosphatase and retains glucose-6-phosphate for glycolysis.
Branching enzyme (amylo-1,6-transglucosidase) transfers segments of α-1,4-linked glucose chains to create α-1,6 branch points in glycogen.
