The endocrine system part 1 Flashcards
lecture 9 week 5
How do hormones move
- hormones are chemical messengers secreted by the endocrine gland
- exocrine glands release hormones via ducts eg.enzymes
- endocrine glands are ductless
the cell of the endocrine tissue release the hormone into the blood stream. the hormone travels in the blood stream to the target cell where the hormone then binds to the receptor
receptors are membrane bound or intracellular
What are the classifications of hormones
peptide hormones: made up of few to many amino acid residues (insulin, glucagon, TRH, FSH)
amine hormones: derivative of specific amino acids (tyrosine: catecholamines and thyroid hormones)
steroid hormones: derivatives of cholesterol (progesterone, testosterone and estrogen)
receptors on peptide and catecholamine hormones on plasma membrane. steroid and thyroid hormones are intracellular
- this depends on whether the hormone can cross the lipidbilayer
How are hormone levels quantified
hormone levels in body fluid can be quantified by immunoassays eg. Enzyme linked immunosorbent assay (ELISA)
What is the hypothalamus
- the master regulator that produces ADH, oxytocin and regulatory hormones
regulatory hormones
- GHRH: growth-hormone releasing hormone
- CRH: corticotrophin releasing hormone
- TRH: thyrotropin releasing hormone
- GnRH: gonadotrophin releasing hormone
What is the feedback mechanism of hormones
- maintains homeostasis: increases or inhibits hormonal secretion
- positive or negative feedback
- negative feedback is common with hormone secretion
eg. Hypothalamus —-> Anterior pituitary gland —> Thyroid gland —> T3 and T4 (thyroid hormone)
Hypothalamus —> Anterior pituitary gland (TRH - thyroid releasing hormone)
Anterior pituitary gland —> Thyroid gland (TSH - thyroid stimulating hormone)
Maintaining glucose metabolism
food is broken down to monosaccharides transported by the portal vein to the liver. glacatase and fructose converted to glucose and excess into fats. fat is then converted to fatty acids and glycerol and used in Krebs cycle excess as glycogen
What is the anatomy of the pancreas
eterocrine gland (acts as endocrine and exocrine gland)
- digestive enzymes into small intestine (exocrine)
- glucagon and insulin (endocrine)
histology
- pancreatic Islets are surrounded by endocrine cells
- alpha-cells form glucagon
- beta cells form insulin
- delta cells make somatostatin
- F cells form pancreatic polypeptides
low glucose
i. low glucose levels in blood
ii. metabolism slows
iii. ATP decreases
iv. Katp channels open
v. cells at resting membrane potential no insulin is released
high glucose
i. high glucose in blood
ii. metabolism increases
iii. ATP increases
iv. Katp channels closes
v. cell depolarisaiton and calcium channels opens
vi. Ca2+ acts as entry into cells
vii. Ca2+ triggers exocytosis and insulin is secreted
What factors control insulin secretion
+ amino acids
+ increased plasma glucose
+ GIP (gastric inhibitry polypeptide - hormone regulating blood glucose levels)
+ glucagon
+ parasympathetic nerve activity
+/ - sympathetic nerve activity
- somatostatin (inhibits insulin release)
What happens to glucose levels after eating
- during fasting blood glucose is relatively low
- after eating, the rise in blood glucose is sensed by pancreatic beta-cells causing insulin to be released
- insulin stimulates the uptake of glucose into tissues, excess glucose to glycogen and fatty acids
Insulin secretion and plasma glucose levels
- insulin release is greater when glucose is injested compared to an intravenous injection
- hormones in GI tract called incretins enhance insulin release
- at high levels of insulin, glucagon level is low as it will trigger the release of more glucose
- insulin release is more proportional to glucose, it is bi-phasic, the 1st release is prepared and then more is made so a gap is seen
How does glucose enter into cells
- glucose enters by facilitated diffusion
- each tissue expresses different GLUTS
- GLUT 1: ubiquitous
- GLUT 2: hepatocytes/beta cells
- GLUT 3: neuron
- GLUT 4: adipose tissue/muscles (insulin dependent)
in the absence of insulin, glucose cannot enter the cell
- insulin signals the cell to insert GLUT 4 transporters into the membrane, allowing glucose to enter the cell
What is the homeostatic control of blood glucose
- insulin vs glucagon
- high levels of glucose increase insulin levels
- the glycemic index shows how food can spike glucose levels in the blood
What is the feedback mechanism for blood glucose regulation
high blood sugar
- more insulin is released from the pancreas, this stimulates glycogen formation and more glucose is converted to glycogen which lowers blood sugar
low blood sugar
- low blood sugar is detected and the pancreas secretes glucagon which stimulates glycogen breakdown, the breakdown forms glucose which raises blood sugar
Information about diabetes
type i diabetes: auto-immune destruction of pancreatic beta-cells, cause is unknown
type ii diabetes: insulin intolerance often obesity-related
treatments: type i: taking insulin injections/pumps. type ii: diet/exercise, hypoglycaemic drugs, post-prandial glucose regulating drugs
diagnosis reference
reference
- fasting (4mM), post prandial (6-7 mM), HbAlc (4-5%)
impaired
- fasting (6-7mM), post prandial (7.9-11mM), HbAlc (6-6.4%)
diabetes
- fasting (>7mM), post prandial (>11mM), HbAlc (>6.5%)
HbAlc - percentage of red blood cells that become glycated
Hyperglycemia
- typical for type i and type ii diabetes
- increased glycolysis
look at flow chart for symptoms
