Worksheet Mteab

Mariel Jane D.
Tagaza 2021-C
INTRODUCTION TO METABOLISM worksheet
CASE 1.
Task 1. Discuss the process involved in the development of obesity in terms of CHO, CHON, lipid
metabolism.
 Adiponectin levels fall, and with it, reduced fatty acid oxidation occurs in tissues. The release of free fatty
acids is also increased in large adipocytes, presumably because of the high concentration of substrate
(triglyceride), even if hormone-sensitive lipase is not activated
 coupled with a deficiency of perilipins (adipocyte phosphoproteins that bind to triacylglycerol droplets
and regulate the accessibility of the triglyceride to the lipases) in obese individuals = enhanced basal rate
of lipolysis
 Increased circulating levels of nonesterified (or free) fatty acids (NEFAs) are observed in obesity and is
associated with insulin resistance.
o As NEFA levels in the circulation rise, muscle begins to use predominantly NEFA as an energy
source
o reduces muscle glucose metabolism, as a result of the buildup of acetyl-CoA in the mitochondria,
export of citrate to the cytoplasm, and inhibition of PFK-1.
o glucose is not being metabolized, its uptake by muscle is reduced
o impaired glucose uptake (resulting from fat oxidation) is manifested as a sign of insulin resistance
Task 2. Discuss the metabolic events involved in energy storage of CHO, protein, lipid.
FATE OF CARBOHYDRATE
 taken up by hepatocytes
 not all utilized; distributed to other cells
 oxidized through glycolysis PDH complex TCA ETC Oxidative Phosphorylation (OP)
 Products: CO2 H2O, ATP
 excess glucose → stored in liver as glycogen via glycogenesis
 stores can reach up to 200-300g
 glucose may enter FA/TAG synthesis
 PDH reaction → acetyl CoA → TAG synthesis
 Liver: glycerol kinase → glycerol
 adipose tissue: no glycerol kinase; TAGs synthesized from glucose
 TAGs packaged in VLDL → extruded to circulation
 organs that depend ONLY on glucose for energy
o Brain
o RBC
o Testes
o Renal medulla
o Iris of the eyes
FATE OF LIPIDS
 Found in blood vessels
 In well-fed state: ↑insulin → stimulate lipoprotein lipase (LPL) → hydrolyze TAGs in VLDL →
↑glycerol, FAs
 Glycerol taken up by liver
 FAs taken up by adipocytes
 In adipose: FAs esterified to glycerol 3-phosphate (from glycolysis pathway)
 All TAG synthesis precursors in adipose come from GLUCOSE.
 ↑carbohydrates → ↑TAG synthesis in adipocytes
 In muscle, some FAs taken up, but glucose most often used as fuel.
 difference in muscle and liver glycogen
 liver: no glucose-6-phosphatase
 muscle: glucose-6-phosphatase present → glycogen stores used in that muscle only
 In RBC: no mitochondria → anaerobic glycolysis only
 Products: lactate, 2 mol ATP
 Lactate to liver → pyruvate via lactate dehydrogenase → to TCA cycle
FATE OF PROTEIN
 AAs are building blocks of proteins.
 Proteins synthesized in liver can be used in liver or elsewhere.
 essential amino acids (PVT TIM HALL) not synthesized; must be present in diet
 nitrogen-containing compounds can be derived from AAs (e.g purines, pyrimidines)
 excess amino acids degraded, not stored
 AAs deaminated in liver via urea cycle
 amino group of amino acids → ammonia (as urea) → eliminated via urea cycle → excreted in the urine
 Urea cycle continuously occurs regardless of nutritional status. It is just the rate that varies.
 AA carbon skeleton of the amino acids can enter glycolysis or TCA
 Enter glycolysis via pyruvate
 Enter TCA via acetyl CoA
Task 3. Explain the organ and cellular and level of function.

CASE 2.
Task 1. Discuss the process involved in the development of a nutritionally deficient individual in terms of
CHO, protein and lipid metabolism.
Task 2. Discuss the metabolic events involved in energy utilization of CHO, protein, lipid metabolism.
Liver, skeletal muscle, adipose: FA oxidation exclusively

 These organs do not undergo glycolysis in order to conserve glucose for brain and RBC.
 ↓need for AA precursors → ↓proteolysis → ↓urea cycle
 Urea cycle will always be active, but rate differs.
 KB synthesis in adipose tissue and skeletal muscle will decrease the use of ketones bodies so that brain
can use it instead.
 ↑KB → cross blood-brain barrier
 in adipose: activation of hormone specific lipase → TAG lipolysis
 In kidney, gluconeogenesis is active
 there are compensatory mechanisms for metabolic acidosis
Task 3. Explain the role of glucagon in starvation.
 In starvation, glucagon secretion is promoted while insulin secretion is reduced, causing elevated blood
glucose levels.
 Glucagon action is mediated by a G protein-coupled receptor (GPCR) that is coupled to adenyl cyclase.
Glucagon also mediates an increase in intracellular calcium in a phospholipase C−dependent manner and
activates AMP-activated kinase and c-Jun N-terminal kinase.
 Activation of the GPCR in hepatocytes mediates the primary actions of glucagon: ketogenesis and
increased hepatic glucose production—glucagon increases the net hepatic glucose output through
increased expression of gluconeogenesis enzyme and glycogen degradation without altering the
gluconeogenesis flux
 Glucagon has potent hypolipidemic actions and reduces triglycerides and very-low-density lipoprotein
release aswell as the deposition of triacylglycerol in the liver, in addition to reducing cholesterol levels
and stimulating fatty acid oxidation

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Mariel Jane D.

Task 3. Explain the organ and cellular and level of function.

Liver, skeletal muscle, adipose: FA oxidation exclusively

Task 3. Explain the role of glucagon in starvation.

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