6 - Getting the balance right in H&D Flashcards
What are the 2 main peptides that are markers of adiposity?
Pancreatic hormone insulin
adipose tissue hormone leptin
How can covalent modification of enzymes affect Vmax?
Enzymes subject to covalent modification undergo phosphorylation by a protein kinase
or dephosphorylation by phosphoprotein phosphatase.
Activates/deactivates enzymes, affecting Vmax
What does the glucagon g-protein coupled receptor activate/produce
Activates adenylate cyclase
activates PKA
cAMP production
Phosphorylation of target enzyme
Phosphorylation of phosphofructokinase 2 (PFK2) inhibits that enzyme’s action and _______ becomes active. As a result ________ is converted to Fructose 6-phosphate. Phosphofructokinase activity ____ and glycolytic rate ____
Phosphorylation of phosphofructokinase 2 (PFK2) inhibits that enzyme’s action and fructose bisphosphatase (FBPase) becomes active. As a result Fructose-2,6-bisphosphate is converted to Fructose 6-phosphate. Phosphofructokinase activity falls and glycolytic rate falls
Give the consequences of a gluconeogenesis disorder
Glucose cannot be synthesized from certain substrates derived metabolically
Patients with severe disease are affected neurologically: low muscle tone; seizures; slow development
Lactic acid is usually elevated chronically
Give the consequences of fatty acid metabolism disorders such as CPT1 deficiency
There may be no obvious symptoms when eating well and otherwise healthy
Symptoms may occur when food intake is inadequate and/or the patient is sick and food intake cannot keep up with demand
Hypoketotic, hypoglycaemic
Lactate serves as a substrate for….__?
Fatty acid synthesis via pruvate and aceyl-coA
Prolonged exposure to high glucose and FFA can cause significant impaired beta cell function and beta cell death as a result of ____ leading to a requirement of ____
chronic gluco-lipotoxicity
requirement for insulin replacement therapy in later stages of T2DM
Why is there no keto-acidosis in type 2 diabetes, unlike type 1?
Small amount of insulin remaining is sufficient to inhibit synthesis of ketone bodies.
What is the state of the liver in type 1 diabetes melitus?
Gluconeogenic and ketogenic
Explain the effect of the Atkins/ketogenic diet on the metabolism.
The liver remains gluconeogenic even in the fed state > dietary amino acids are used to produce glucose and glycogen (still activated by low levels of insulin). Ketone bodies produce ATP for gluconeogenesis. Fatty acids are utilised by the liver and muscle.
Why does the Atkins/keto diet not produce acidosis in the ‘starved’ state when type 1 diabetes does?
Diabetes type 1 produces high levels of glucose and ketone bodies in the blood, whereas the ketogenic diet results in a net reduction in glucose, and the ketones are utilised by perpheral tissues, preventing acidosis.
HIF-1a is produced by core tumour cels. What are their effects?
Hypoxia-inducible factor (a transcription factor)
and is the enzyme responsible for the inhibition of the pyruvate deydrogenase complex (PDK1) prevents entry into TCA cycle
Effectively ‘shuts down’ mitochondrial respiration
Leads to Increased expression of glucose transporters and glycolytic enzymes - warburg effect (a switch to anearobic glycolysis)
What diet is recommended in kidney failure cases and why?
Diet high in carbohydrate and low in protein is essential to ensure that the liver utilizes ammonia to synthesize non-essential amino acids from TCA cycle intermediates, allowing a reduction in urea output from the liver.
Alpha keto glutarate + NH4+ = Glutamine
