Diabetes Mellitus Biochemistry PDF

Capillary membrane changes (due to protein glycosylation) **Microvascular Diseases** leading to retinopathy and nephropathy (D-...

Capillary membrane changes (due to protein glycosylation) **Microvascular Diseases** leading to retinopathy and nephropathy (D- glucose, L-sorbitol accumulation) It is Balance of glucose production and utilization Large vessel disease: gangrene, ulcers, **Macrovascular Diseases** atherosclerosis Promotes glycogen storage **Glucose Homeostasis** **Insulin** (lowers blood glucose) Abnormal glucose metabolism in nerve cells Enhances glucose uptake in tissues **Neuropathies** **Long-Term Complications of Sorbitol accumulation → Schwann cell injury Diabetes** **Glucagon** (raises blood glucose) Stimulates glycogenolysis and gluconeogenesis develops due to increased glomerular filtration **Renal Failure** rates and sorbitol accumulation Insulin activates enzymes that convert glucose Glycogen synthesis Vascular inflexibility to glycogen for storage **Chronic Insulin Elevation Effects** Hypertension risks Insulin stimulates amino acid uptake for protein **Anabolic process activated by insulin Effects** Protein and lipid synthesis synthesis and fat storage Insulin assists in the cellular uptake of ions like Ion absorption (K+, PO4^3-) extracted from pigs and cows or produced by potassium (K+) and phosphate (PO4^3-) Insulin injections bacteria The process of making glucose from non- Gluconeogenesis Hypoglycemia is a risk, and glucose levels must carbohydrate sources is reduced **IDDM Treatment** be carefully monitored **Metabolic Effects of Insulin** Glycogenolysis Emergency hypoglycemia treatments: oral Breakdown of glycogen and fat is minimized glucose, glucagon, glucose injection **Diabetes Treatment** **Inhibitory Effects of what glucagon activates Lipolysis ** (on catabolic pathways) Diet adjustments (low fat, high fiber) Ketogenesis Insulin inhibits ketone body formation and **NIDDM Treatment** Oral medications to improve insulin sensitivity protein breakdown Proteolysis and secretion Secretion of too much Glut 4 transporters that transport glucose to muscle cells and adipocytes This diagnostic test assesses how well the body manages a glucose load After fasting, a specific amount of glucose is Diabetes Mellitus Insulin-dependent administered, and blood glucose levels are measured over time **Oral Glucose Tolerance Test** Biochemistry Mind Autoimmune destruction of pancreatic beta Normal and diabetic response curves show Map **Type I Diabetes (IDDM)** (in dogs its more common (in older dogs)) cells differences in glucose clearance, with diabetic Typical onset: young age patients showing prolonged elevation above 11.1 mmol/L at 120 minutes Requires insulin injections **Types of Diabetes** Non-insulin dependent, insulin resistance Type II diabetes differs from Type I in that **Type II Diabetes (NIDDM)** (in cats its more insulin is present but cells resist its effects Typical onset: older age, often linked to obesity common) Reduced glucose utilization in peripheral tissues Managed with diet, exercise, and hypoglycemic agents (Ketoacidosis is uncommon in Type II due to some functional insulin, which prevents severe Low risk of ketoacidosis **Insulin Resistance** lipolysis and ketogenesis) **Diabetes Mellitus Type II (NIDDM) Pathophysiology** **IDDM**: Lack of insulin, resulting in high blood glucose and ketone bodies Insulin resistance primarily impairs glucose Hypertriglyceridemia occurs **Glucose Utilization: IDDM vs utilization in muscle and fat tissues NIDDM** **NIDDM**: Insulin resistance but no severe lipolysis or ketoacidosis Glycosuria Dehydration and worsening insulin resistance **Hyperglycemia Effects** results in energy mobilization from glycogen and Increase Catabolic state No glucagon activity fat stores increase, leading to high glucose and amino acid **Insulin Deficiency** Increased gluconeogenesis, proteolysis levels in the blood Decreased insulin/glucagon ratio because no Glut 4 stimulated by insulin. SO not leads to hyperglycemia ↓ Glucose uptake by tissues Reduced glucose utilization used by muscle cell and adipocytes ↓ Glycolysis **Diabetes Mellitus Type I (IDDM) Lipolysis and impaired fat absorption lead to ketone body further elevate blood glucose **IDDM: Metabolic Alterations** Pathophysiology** Lipolysis → Ketogenesis → Ketoacidosis production, resulting in ketoacidosis ↑ Gluconeogenesis Hyperglycemia Increased ketogenesis results in high ketone body levels, contributing to acidosis and ↑ Lipolysis and ketogenesis Effects: glucose is so high that the kidney can't absorb potential coma if untreated **Metabolic Effects** Polyuria (glucose in urine) everything, so it gets ride of it in the urine cause tissue breakdown ↑ Proteolysis Dehydration and electrolyte loss ↑ Blood levels of glucose, fatty acids, ketone because lipoprotein lipase which is stimulated by bodies Increase in triglycerides insulin is not produce. And it synthetize TG into the adypocide. So there is a increase in TG