Metabolic processes of kidneys Flashcards
what are the different processes at the renal cortex and medulla
how does structure relate to function
- renal cortex = gluconeogenesis
- structure: greater blood supply and cells have more mitochondria
- more oxygen for mito to have AEROBIC respiration
- more ATP produce to sustain high energy process such as gluconeogenesis - renal medulla = glycolysis
- oxidation of glucose = pyruvate
- less energy demand - less blood flow to regions
what is the renal threshold of glucose absorption and briefly explain its implication
- GFR: 90-140 ml/min
- glucose all freely filtered (amount filtered is linear to plasma concentration)
- all reabsorbed UNTIL renal threshold reached
this usually happens at the plasma level of 11mmol/L AND at the rate of 375mg/min
- when this threshold is exceeded, GLUCOSE will be found in URINE (glucosuria)
describe the process and location of glucose reabsorption from filtrate
at PROXIMAL tubule
- LUMEN side: SGLT1 and 2 - mostly SGLT2
- 2 active transport, using Na gradient - BASOLATERAL side: GLUT1 and GLUT 2
- fascilitated passive diffusion - bidrectional
- GLUT1 = early segment, GLUT2: later segment
why do diebetic have increased renal TH for glucose
- increased expression of SGLT2 = more reabsorbed into blood = maintains hyperglycaemia
SGLT2 inhibitor = can inhibit this process but produces glucosuria
GFR, plasma glucose and renal TH
High GFR = less plasma glucose concentration to reach renal threshold
opposite for low gfr
what are the 2 hormones that regulate renal gluconeogenesis
insulin: inhibits
catacholamine: PROMOTES renal gluconeogenesis hence release
glucagon no influence
what are the 2 substrates for renal gluconeogenesis
glutamine = muscle source, glutamate (cytosolic conversion to glutamine in most cells)
lactate
describe the reciprocal hepatorenal release of glucose
FED state:
KIDNEY predominantly makes glucose and releases glucose to sustain body (contribute 60%)
- glucose in liver is converted to glycogen and stored
FASTED state:
LIVER predominantly makes glucose and releases (80%)
- 50% glycogenolysis, 50% gluconeogenesis
Kidney: gluconeogenesis only
how does acidosis and liver disease affect the hepatorenal relationship in glucose release
Liver disease: body wont lack glucose (no hypoglycaemia), as kidneys can take over and release
Acidosis, especially diabetic acidosis:
low pH environment enhances muscle glutamine release = more substrate - renal -neo AND stimulate renal gluconeogenic pathway
INHIBIT LIVER gluconeogenesis
= MORE RENAL RELEASE
Glutamine metabolism product and their uses
- deamination = NH3 produced, used as H buffer in URINE (ammonia formed)
- a-ketoguterate
used as fuel - into TCA cycle produce ATP and CO2
gluconeogenesis - produces GLUCOSE
pathologies that interfere with glutamine handling
1 acidosis: increased glutamine availability AND more catabolised
- normal acid base: glutamine MOSTLY REABSORBED into blood
how does type 2 diebetic affect renal gluconeogenesis in fast and fed state
increases -neo in BOTH states because
- insulin insensitve
- impaired insulin release
- substrate level
- enzyme activation
what does the kidney do with glucose
- glycolysis
2. glycogen synthesis - glycosylation of proteins