Biochemistry Lecture Notes PDF

Lec. F Semester 3 Biochemistry GONA KAMAL ALI MSc. Biomedical and clinical lab analysis  Integration of Metabolism in Normal and Abnormal Conditions Metabolic Integration Regulation of metabolism in different physiolo...

Lec. F Semester 3 Biochemistry GONA KAMAL ALI MSc. Biomedical and clinical lab analysis  Integration of Metabolism in Normal and Abnormal Conditions Metabolic Integration Regulation of metabolism in different physiological states. Relevance to Dentistry: Implications for oral health and systemic conditions.  Roles of Insulin and Glucagon in the Well-Fed State Insulin: Released from pancreatic beta cells in response to high blood glucose. Promotes glucose uptake by cells, glycogenesis, and lipogenesis. Glucagon: Released from pancreatic alpha cells in response to low blood glucose. Minimal role in the well-fed state due to high insulin levels.  Biochemical Alterations in the Well-Fed State Carbohydrate Metabolism: Increased glucose uptake and storage as glycogen in liver and muscle. Enhanced glycolysis and suppression of gluconeogenesis. Lipid Metabolism: Increased fatty acid synthesis and triglyceride storage in adipose tissue. Protein Metabolism: Increased protein synthesis and reduced protein degradation.  Biochemical Alterations During Fasting Shift to Catabolic State: Decreased insulin, increased glucagon. Carbohydrate Metabolism: Glycogenosis and gluconeogenesis in the liver to maintain blood glucose levels. Lipid Metabolism: Increased lipolysis in adipose tissue, leading to fatty acid release and ketogenesis. Protein Metabolism: Increased protein degradation to provide substrates for gluconeogenesis.  Biochemical Alterations During Exercise Initial Phase: Increased glycolysis and glycogenolysis for rapid ATP production. Prolonged Exercise: Increased fatty acid oxidation as a sustained energy source. Hormonal Regulation: Increased catecholamines, decreased insulin, and increased glucagon.  Roles of Insulin and Glucagon During Starvation Insulin: Low levels due to reduced blood glucose. Glucagon: High levels promote gluconeogenesis and ketogenesis. Adaptation: Body shifts to using ketone bodies and fatty acids as primary energy sources.  Biochemical Alterations During Starvation Carbohydrate Metabolism: Depletion of glycogen stores. Gluconeogenesis from non-carbohydrate sources. Lipid Metabolism: Increased lipolysis and ketogenesis. Protein Metabolism: Proteolysis to supply amino acids for gluconeogenesis.  Biochemical Alterations in Type I Diabetes Mellitus Insulin Deficiency: Autoimmune destruction of pancreatic beta cells. Metabolic Consequences: Hyperglycemia, increased lipolysis, ketoacidosis. Clinical Manifestations: Polyuria, polydipsia, weight loss, diabetic ketoacidosis (DKA).  Biochemical Alterations in Type II Diabetes Mellitus Insulin Resistance: Cells become less responsive to insulin. Metabolic Consequences: Hyperglycemia, hyperinsulinemia, dyslipidemia. Clinical Manifestations: Obesity, hypertension, increased risk of cardiovascular disease.  Metabolic Response to Injury Acute Phase Response: Increased cytokine production (e.g., IL-6, TNF-alpha). Metabolic Changes: Hypermetabolism, increased protein catabolism, gluconeogenesis. Clinical Implications: Muscle wasting, hyperglycemia, impaired wound healing.  Implications for Dentistry Oral Manifestations: Poor wound healing, increased infection risk in diabetics. Dental Management: Careful monitoring of diabetic patients, managing metabolic disorders.