Physiology 👩⚕️unit 1 > Study Guide Chapter 22 Metabolism And Glucose Regulation > Flashcards
Study Guide Chapter 22 Metabolism And Glucose Regulation Flashcards
Metabolism
The sum of all chemical reactions in the body
Anabolic/catabolic
Anabolic: build large from small catabolic: break down large into small
Pathways
Directly or indirectly
Energy balance
Energy and is equal to energy out or you will gain or lose weight
Glycogen
Storage of carbs and muscle tissue
Two states of metabolism
Fed state & fasted state
Fed state
absorptive state just eaten building molecules
Fasted state
Post absorptive breaking down glycogen/fat
Glycogenesis
Synthesis of glycogen
Lipogenesis
Synthesis of lipid builds fat
Glycogenolysis
Breaking down of glycogen
Glyconeogenesis
Synthesis of new glucose from other molecules example amino acids
Push pull control
Metabolism is controlled by push pull can work equally or unequally.
Polyphagia
Over eating
Osmotic diuresis
Loss of water in urine due to reabsorbed salutes by PCT in nephrons
Polyuria
Excess urinating
Glucosuria
Glucose in urine
Polydipsia
Excessive drinking
Metabolic acidosis
Caused by anaerobic metabolism and in type one diabetic‘s produce Keytone bodies
Keto acidosis
Proteins/fat metabolism: related to weight loss and leading to keto acidosis
Keytone bodies
Conversion of excess fatty acids formed in fat metabolism. Signs include high ventilation rate, urine acidification, hyperkalemia ( high potassium and blood)
Describe methods for measuring metabolism metabolic rate. What factors influence metabolism
Factors that influence metabolism: age, sex, activity, lean muscle mass, diet, genetics, hormones. Metabolism is the sum of all chemical reactions in the body the anabolic and catabolic pathways, synthesize and breakdown of molecules. Measured indirectly by calorimetry example O2 consumption or CO2 production. Directly measured through bomb Calometry, food caloric values an amount of heat produced when burned is measured
Describe the overall metabolic process occurring during fed state. Including insulin and glucagon whole body glucose regulation
A.k.a. observant of state: follows meal when molecules from food are absorbed and undergo anabolic pathways to build high energy compounds or store them. Whole body glucose goes up, insulin goes up, glucagon goes down, Glycogenesis goes up glycogenolysis goes down, glycogen synthesis.
**white board **
Describe the overall metabolic process occurring during fasted state. In particular explain the roles of insulin glucagon and whole body glucose regulation
A.k.a. post absorptive state:. When nutrients from food are not available and body uses catabolic pathways to break down start molecules for energy. Whole body glucose goes down, insulin goes down, glucagon goes up, GlycoGenesis goes down, glycogenolysis goes up, glucose synthesis
white board
Listen describe the cellular make up of pancreatic islets of Langerhans
1) Beta cells 75% produce insulin,
2) alpha cells 20% produce glucagon,
3) d cells produce somatostatin decrease gastrin secretion in stomach,
4) PP cells aka F cells secrete pancreatic polypeptide function not clearly understood
List and describe the cellular actions of insulin
- Glucose oxidation goes up glycolysis cellular respiration ATP is produced.
- glycogenesis goes up 
- Lipogenesis goes up
- Proteins synthesis goes up
Listen describe the cellular actions of glucagon
- Glycogenolysis goes up -gluconeogenesis goes up
- Ketogenisis goes up (break down of protein)
Explain the normal presence/ratio of insulin and glucagon on glucose regulation
Varying ratio. 90 mg/dL fasted plasma glucose. 140 mg/dL after meal plasma glucose. Insulin secreted when glucose is greater than 100 mg/dL by beta cells
List and describe the processes involved with insulin secretion. Which cells produce/secrete insulin and what are the target sells?’s which sell ask independently of insulin to take up Glucose
1) Plasma glucose greater than 100 mg/dL
2) Increase plasma amino acid
3) Feed forward affect of G.I. hormone released by small intestine or other anticipation of glucose surge
4) ANS: sympathetic/parasympathetic activity prevent or stimulate secretion. Secretion by beta cells primary target for insulin are liver cells Hepatocytes, adipose issue, skeletal muscle. small intestine act independently will take up glucose as well as brain
List and describe the mechanistic, molecular level actions of glucose regulation by insulin compare these actions between adipose skeletal and hepatic tissue
Both Happen via Tyrone kinase receptor enzyme pathways
* individual slides for each
Adipose/resting skeletal muscle glucose regulation by insulin
Happens via Tyrone kinase receptor enzyme pathway. direct insulin binds to Tyron kinase receptor, signal transduction cascade starts. Intracellular GLU4 transporters are inserted into cell membrane via exocytosis. Glucose enters cell via facilitated diffusion, down concentration gradient.
Hepatic tissue glucose regulation by insulin
Happens via tyrosine kinase receptor enzyme pathway. Indirect liver cells. GLUT 2 transporter reside in cell membrane transporting glucose into plasma. Insulin binds to Tyrosine kinase receptor, signal transduction cascade starts. Signal cascade activates hecto kinase, which converts intracellular glucose to G6P keeping glucose low and extra cellular glucose diffuses into the cell
List and describe the processes involved with glucagon secretion. Which cells produce/secrete glucagon and what are the target cells 
1) Plasma glucose drops below 100 mg/dL
2) plasma amino acids go up (which is weird the same signal from insulin secretion) * so Pro Tien meal would still stimulate the release of glucose.
3) Secretion is modulated by insulin and glucose uptake By alpha cells.
Target cells for glucagon are liver hepatocytes
List the four effects of glucagon
1) increase blood glucose via glycogenolysis 75%
2) Increase blood glucose via glyconeogenesis 25%
3) Increase Gene expression of glyconeogenesis proteins
4) Increase Lipo licenses for keto neogenesis ( ketones for brain function)
List and describe the Mechanistic, molecular level actions of glucose regulation by glucagon
Glucagon increase his plasma glucose mechanistically at a molecular level through GPCR adenylyl cyclase CAMP system.
1) Glucagon binds with receptor G Pro Tien activated, moves to adenylyl cyclase, activates it ,and AC converts ATP to cAMP
2) Camp amplifies a signal by activating PKA, activation of enzyme for glycogenolysis and gluconeogenesis and inhibition of enzymes for glycogenesis and glycolysis
Describe diabetes mellitus in general terms and specify forms of DM. What is the prevalence in the US and what are the main causes?
A family of metabolic disease is associated with pancreatic and a cream puff theology. Estimated to affect 9.3% of US population with 37% Of the population affected with pre-diabetes. Primary linked to sedentary lifestyle, over eating and obesity. Characterized by hyperglycemia can affect blood vessels eyes kidneys and nervous system. Type one diabetes 10% of cases insulin deficiency do the distraction of beta cells by the immune system. Type two diabetes 90% of cases insulin resistant, insulin is released by receptors are desensitize due to constant presence of insulin. Later and disease may become dependent on insulin injection
Listen describe the signs and symptoms and diagnostic test of diabetes. What are considered normal, pre-diabetic, and diabetic glucose levels for each test
Signs and symptoms: thirst, constant urination, weight loss. Diagnosis has two methods. Neither can distinguish the form of DM.
1) Testing plasma glucose levels after eight hour fasting, normal glucose levels are less than 100 mg/dL, pre-diabetes are 100 to 125 mg/dL, diabetes levels are 125 mg/dL.
2) Glucose tolerance test: I personally drink solution of 75 g of dissolved glucose, plasma glucose is measured every 30 minutes for two hours. Normal levels are less than 140 mg/dL‘s after two hours, pre-diabetes are 140 to 199 mg/dL, diabetes are greater than 199 mg/dL
Describing him for the detailed causes and symptoms of type one and type two diabetes. What treatments are available for each
Type of one: genetically linked or sometimes caused by viral infection, person is reliant upon insulin injections, without insulin cells go into facet state metabolism. Type 2 : Usually a thing to obesity, with some genetic overlap and age relation, growing frequently among children and adolescents. Person cells are typically insulin resistant due to the sensitization of receptors but may also have decreased insulin secretion, leading to hyperglycemia but also rise glucagon secretion by insulin desensitization.
Symptoms may not be as severe as type one, but lied to atherosclerosis, renal failure, blindness last day from cardiovascular disease. Treatment as their lifestyle change exercise and diet also drugs
