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HW9-Metabolism 2
HW9-Metabolism 2
Citrate levels can be maintained through the flux of glutamine-derived α-KG, which is carboxylated to
isocitrate and citrate by the mitochondrial isoform of IDH2. This mitochondrial flux can be accomplished
by NADH conversion to NADPH by mitochondrial transhydrogenase and the resulting NADPH use in α-KG
carboxylation. This the enzyme that influence the metabolic rate of citrate in the mitochondria.
When cytosolic pyruvate is reduced by cytosolic NADH, less ATP is produced. This is because per
cytosolic NADH, less quantity protons are pumped than per matric NADH.
Obesity is a complex disease that can lead to critical conditions due to the excessive amount of fat found
in the body. Meanwhile, there is a hormone that plays an imperative role in weight regulation that’s
primarily produced by the fat tissue. This hormone is known as leptin.
Leptin reduces food intake and body weight, the coexistence of prominent leptin levels with obesity is
widely interpreted as evidence of leptin resistance. This hormone has been allowed for lipodystrophy.
This prevents the reduction in metabolic rate that is associated with weight loss.
In conclusion, yes, it is possible to use leptin for treating obesity associated with congenital leptin
deficiency.