Lipid metabolism and metabolic disorder

Lipids

Lipids

triglycereide,phospolipid, steroids

fat/triglyceride

type of lipid, source of energy

excessive hepatic ketone synthesis as a result of low insulin and high glucagon/epinephrine

what leads to diabetic ketoacidosis

acetoacetate, acetone, 3-hydroxybutyrate

products of ketogenesis

acetoacetate and 3-hydroxybutyrate

products of ketogenesis transported in blood to peripheral tissue and reconverted to Acetyl CoA

adipose tissue

where are lipids stored

liver

where are lipids produced

saturated

which lipid is more tightly packed

saturated

which type of fat increases LDL

enzyme inhibition in citric acid cycle

what stops citric acid cycle during high ATP

citrate

what molecule accumulates to be fed into lipid synthesis

high ATP/ high insulin

under what conditions is citrate stopped from continuing the citric acid cycle

citrate shuttle

transports citrate from mitochondria to cytoplasm

acetyl coA

what is citrate converted into in cytoplasm to undergo lipid synthesis

palmitate

3rd step of fatty acid synthesis, most common FA, acetyl coA and malonyl group

linolenic acid

precursor to omega-3

linoleic acid

precursor of omega-6

oleic acid

body makes minute amount conditionally essential fatty. acid

arachidonic acid

important for prostaglandin and thromboxane synthesis, essential only in deficiency of linoleic acid (linoleic acid is a precursor)

cyclooxygenase pathway

pathway that forms prostaglandins, prostacyclin, thromboxane

NSAIDs

inhibits cyclooxygenase (COX) pathway

aspirin (NSAIDs)

inhibits synthesis of thromboxane

bile salts

aids in lipid absorption, formed from cholesterol in liver, absorbed in ileum, stored in gall bladder

chylomicron

lipoprotein carrying lipids from gut to capillaries of muscle

lipoprotein lipase (LPL)

catalyzes break down of chylomicron into fatty acids

apo CII

activates LPL( lipoprotein lipase)

LPL/APo CII deficiency

leads to accumulation of chylomicron in plasma, increased risk of acute pancreatitis (inflammation in pancreas) causing abdominal pain

VLDL

carries fat that body synthesizes

liver

where is VLDL produced

non alcoholic fatty liver

imbalance of hepatic TG synthesis and secretion of VLDL, often associated with obesity and type II diabetes

metabolic dysfunction-associated steatotic liver disease (MASLD)

another name for non-alcoholic faatty liver disease

xanthomas

accumulation of fats under the skin that are not stored properly appears as yellow bumps as a result of LPL/APO II deficiency

HMG CoA reductase

activated by insulin, inhibited by glucagon and statin drugs

HMG CoA reductase

where does statin drug target in cholesterol synthesis

acetyl coA, HMG CoA, mevalonate

cholesterol synthesis important interemeediates

eicosanoids

derivatives of arachonic acid, cyclooxygenase pathway

lipase

breaks down triglyceride into glycerol and fatty acids

glycerol kinase

enzyme that catalyses conversion of glycerol to glycerol-3-P during triglyceride lypolysis in order to make new glucose

beta oxidation

oxidizing and releasing acetyl CoA from fatty acids to produce energy, acetyl CoA into citric aacid cycle, NADH and FADH to ETC

carnitine shuttle

helps transport fatty acids to mitochondrial matrix for beta oxidation in order to produce energy and acetyl CoA

insulin inhibits carnitine shuttle

how does insulin impact carnitin shuttle

hypoglycemia (low blood sugar)

result of carnitine shuttle not working properly

ATP production, FA synthesis, cholesterol synthesis, ketone body synthesis

metabolc fate of aceyl coA

HMG CoA reductase

important enzyme cholesterol synthesis

during period of prolonged starvation when glucose is not available for brain

when might acetyl CoA be converted to ketone bodies

no glucose uptake in brain, pyruvate dehydrogenase (PDH) inhibited, Protein spared

when are ketones metabolized to acetyl CoA in the brain

low insulin high glucagon/epinephrine

under what conditions does ketone metabolism occur

ketoacidosis

toxic affect of over production of ketone bodies

ketolysis

thiophorase important enzyme, breaking down ketones to acetyl CoA for use as energy in muscle,

thiophorase only present in muscle

why cant liver use ketone as fuel

gaucher’s,Niemann-pick, tay-sachs, fabry’s, krabbe’s

diseases that stem from defective lipid metabolism

essential fatty acids (linoleic,linolenic)/ prostaglandins as a result

type of lipid what would be the most deficient during fat-free diet

carnitine shuttle

deficiency in what would cause hypoglycemia, elevated free FAs, low fatty acyl carnitine, and low ketone bodies

defective lipoprotein lipase

cause of chlomicronemia (chylomicron buildup), and xanthomas

sterols

This class of insoluble lipid has fused rings in its structure, is a key component of cell membranes, and functions as a precursor to Vit D