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Carbohydrate metabolism 2 l Biochemistry MCQs

Carbohydrate metabolism 2 l Biochemistry MCQs(multiple choice question) for dental students

ام سي كيو بيو , ام سي كيو كارب , ام سي كيو بيو كيمستري , ام سي كيو طب اسنان ,MCQs for dentistry

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INTEGRATION OF METABOLISM

a Metabolism is defined as the sum total of all chemical reactions that are taking place in the body. It includes the process by which cells use food material to obtain energy, store axcess calorie for future use and build up various substances. Metabolic pathways fall into three categories.

  1. Anabolic pathways:- Involved in synthesis of larger and more complex compounds from smaller precursors, e.g. synthesis of protein from amino acids, triglyceride synthesis, cholesterol synthesis, etc.
  2. Catabolic pathway:- Involved in the breakdown of larger molecules 99, commonly involving oxidative reaction. They are exothermic reactions producing reducing equivalents and mainly via the ETC, ATP. Example are glycolysis, B-oxidation of fatty acid etc.
  3. Amphibolic pathway:-occur at the "crossroads" of metabolism, acting as links between the anabolic and catabolic pathways, eg. the citric acid cycle.

Anabolic and catabolic pathway for all major biomolecules such as carbobydrates, lipids and proteins are intricately linked and well coordinated. There are several crossroads among metabolic pathway, which help in the flow of key metabolites.

 While metabolic pathways of biomolecules are already discussed in previous chapters, this chapter deals with the metabolic interrelationships and the flow of metabolites from ore pathway to another. These aspects are specially important for following metabolic conditions.

  1. Fed state (high insulin: glucagon ratio)
  2. Starvation und diabetes (high glucagon: insulin ratio)

FED STATE (ARSORPTIVE STATE)

a Fed State (absorptive state) refers to the period (2-4 hours) following u meal and is characterized by high levels of nutrients in the blood. There is high level of blood glucose which stimulates the secretion of insulin and inhibits the secretion of glucagon. This results in high insulin: glucagon ratio, High insulin level will cause all the effects which you expect in well fed state with sufficient glucose available:

  1. I) Stimulation of glycolysis:- As there is more glucose, it should be oxidized to obtained energy. So, glucose is immediately converted to glucose-6-phosphate which enters glycolysis.
  2. II) Inhibition of glycogenesis : As glucose is already present in abundance, there is no need to synthesize it from non-carbohydrate source.
  3. III) Stimulation of glycogenesis :- Excess of glucose should be stored as glycogen. Thus, glacose-6-plosphate to glycogen conversion is favoured
  4. IV) Inhibition of glycogenolysis:- There is no need to derive glucose from głycogen stores as it is already present in blood
  5. v) Stimulation of HMP shunt :- Increased availability of glucose-6-phosphate combined with use of NADPH in lipogenesis, stimulate the HMP. This pathway accounts 5-10% of glecose-6-phosphate utilization,      -          Thus, glucose-6-phosphate has three fates in fed state: (i) utilized in glycolysis. (ii) synthesis of glycogen , (iii) utilized in HMP shunt
  6. vi) Stimulation of TCA cycle :- Increased substrate concentration (acetyl-CoA and oxaloacetate) increases the rate of TCA cycle.
  7. vii) Increased lipogenesis , triglyceride synthesis and cholesterol synthesis:- More pyruvate is formed from glucose via glycolysis and is converted to acetyl-CoA. Excess of acetyl-Co is used for synthesis of fatty acids and also cholesterol. Synthesized fatty acids are used to synthesized more triacylglycerol in liver (which incorporate them to VLDL and releases into blood) and adipose tissue (which stores TGs)
  8. viii) Inhibition of B-oxidation:- As acetyl-CoA is already present (from metabolism of glucose) which can be used for generation of energy via TCA cycle, there is no requirement for fatty acid oxidation to generate acetyl-CoA. Further, it will be futile to have fatty acid degradation and fatty acid synthesis occurring at the same time. Therefore, malonyl-CoA (an important substrate of fatty ocid synthesis) inhibits fatty acid oxidation by inhibiting carnitine palimitoyl-tranferase I which transport acyl-CoA from cytosol to mitochondria.
  9. ix) Inhibition of lipolysis (TGs hydrolysis) :- As glucose is already available for most of the tissues as a source of energy there is no need for triacylglycerol hydrolysis to generate free fatty acids as a source of energy.
  10. x) Decrease in ketogenesis : Because acetyl-CoA (substrate of ketogenesis) is diverted towards fatty acid synthesis and TCA cycle, ketone body are not produced.
  11. xi) Increased lipoprotein degradation:- Increased lipoprotein lipase activation releases more fatty acids and glycerol from metabolism of TGc of chylomicrons and VLDL. Fatty acids are taken up by tissue (adipose tissues) for synthesis of TGc.
  12. xii) Increased preteen biosynthesis and decreased protein degradation:- Insulin causes increased amino acid transport across the membrane and also their transamination.

  •          During fed state, glucose is the major source of energy sparing other (e.g. fatty acids) to be stored as energy reserve,

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