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Protein and Lipid Metabolism Prework
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Status
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Published
09/10/2023
What is the rate-limiting enzyme of the urea cycle? {{c1::Carbamoyl phosphate synthetase I}}
Published
09/10/2023
Arginine may be broken down into {{c1::ornithine}} and {{c1::urea}} via the enzyme {{c3::arginase}}
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09/10/2023
Our kidney cannot deal with {{c1::ammonia}}, so the {{c2::liver}} has to come to the resue
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09/10/2023
When amino acids are metabolized, the {{c1::nitrogen}} is formed into {{c2::ammonia}}
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09/10/2023
The urea cycle converts ammonia into {{c1::urea}}
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09/10/2023
After the urea cycle, the urea is shunted to the {{c1::kidney}} where it is expelled from the body
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09/10/2023
There are 2 ways that ammonia can get to the liver{{c1::Glutamine synthetase}} adds ammonia to glutamate, forming glutamine which then travels through…
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09/10/2023
Ammonia enters the liver cell as {{c1::glutamate}}, regardless of the pathway that it takes to get to the hepatocytes
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09/10/2023
Glutamate in liver cells can encounter {{c2::glutamate dehydrogenase}}, converting it into {{c1::alpha ketoglutarate + ammonia }}
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09/10/2023
Glutamate has another option in the liver, it can encounter {{c2::AST}}, forming {{c1::aspartate and alpha-ketoglutarate}}
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09/10/2023
{{c1::Aspartate}} is the only amino acid that can enter the urea cycle
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09/10/2023
The first 2 steps of the urea cycle takes place in the {{c1::mitochondria}}, and the rest happen in the {{c2::cytoplasm}}
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09/13/2023
The inputs of the urea cycle are {{c1::ammonia}}, {{c1::CO2}}, and {{c1::2 ATP molecules}}
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09/10/2023
In the first step of the urea cycle, {{c1::CPS1}} converts 2 ATP + CO2 + Ammonia -> {{c2::carbamoyl phosphate}}
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09/10/2023
{{c1::N-acetylglutamate}} allosterically activates {{c2::CPS1}}, modifying the physical shape of the enzyme so it can process ammonia more efficiently
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09/13/2023
N-acetylglutamate is made by {{c1::N-acetylglutamate synthetase::enzyme}}
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09/10/2023
In the second step of the urea cycle, {{c1::ornithine transcarbamoylase}} combines ornithine with carbamoyl phosphate to form {{c2::citruline}}, relea…
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09/14/2023
Deficiency of {{c1::ornithine transcabamoylase}} is the most common genetic cause of hyperammonemia
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09/10/2023
In the 3rd step of urea cycle, argininosuccinate synthetase combines {{c1::aspartate}} + {{c1::citrulline}} + {{c1::ATP}} to form argininosuccinate
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09/18/2023
The enzyme argininosuccinate lyase breaks up argininosuccinate into {{c1::fumarate}} + {{c1::arginine}}
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09/10/2023
The fumarate that is formed in the urea cycle gets transformed into {{c1::malate}} -> {{c1::oxaloacetate}} -> {{c2::aspartate}}
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09/10/2023
The arginine that is generated in the urea cycle is broken down by arginase to make {{c1::urea}} + {{c1::ornithine}}
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09/10/2023
{{c1::Small, non-polar}} molecules are able to diffuse rapidly through the cell membrane while {{c2::small, polar}} molecules can cross slower
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09/10/2023
{{c1::Large, nonpolar}} molecules (like vitamin A) are able to cross the cell membrane slowly while {{c2::large, polar}} or {{c2::charged}} molecules …
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09/10/2023
Large, polar molecules or charged molecules use {{c1::transport proteins}} to get across the cell membrane
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09/10/2023
There are 2 forms of bulk transport: {{c1::endocytosis}} and {{c1::exocytosis}}
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09/10/2023
{{c1::Phagocytosis}} is a type of endocytosis where WBCs extends pseudopods around the material/cell to engulf it, forming the {{c2::phagosome}}
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09/10/2023
In phagocytosis, an electron pump uses ATP to pump H+ into the phagosome, {{c1::lowering}} the pH
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09/10/2023
The phagosome and the lysosome fuse to form the {{c1::phagolysosome}}
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09/10/2023
After phagocytosis, the lysosome heads to the cell membrane to expel the contents into the {{c1::extracellular space}}
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09/10/2023
Pinocytosis is a type of endocytosis that is {{c1::non-specific}} and takes in {{c1::solutes}}Then, the {{c2::motor proteins (kinesin and dynein)}} ca…
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09/10/2023
{{c1::Receptor mediated endocytosis}} is when special receptors in pits on the cell membrane bind their ligand, causing the edges to come together and…
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09/10/2023
After the vesicle pinches off in receptor mediated endocytosis, the clathrin returns to the {{c1::cell membrane}}
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09/10/2023
In receptor mediated endocytosis, the vesicle merges with the {{c1::endosome}} which is at low pH, causing the LDL to separate from the {{c2::LDL rece…
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09/10/2023
In LDL receptor mediated endocytosis, 2 vesicles form from the endosome. The one with the {{c1::LDL}} goes to the lysosome for digestion and the one w…
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09/10/2023
{{c1::Exocytosis}} starts in the golgi and packages the products from the rough and smooth ER into secretory vesicles which are transported by {{c2::m…
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09/10/2023
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09/10/2023
Net reaction of glycolysis:{{c1::1 glucose}} -> {{c2::2 ATP}} + {{c2::2 NADH}} + {{c2::2 pyruvate}}
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09/13/2023
Glycolysis happens in the {{c1::cytoplasm::cellular organelle}}
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09/10/2023
In response to high blood glucose, the {{c1::pancreatic beta-}}cells secrete insulin
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09/10/2023
Glucose uses {{c1::GLUT transporters}} to get into the cell
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09/10/2023
Glucose is prevented from diffusing out of the cell by {{c1::kinases}} which phosphorylate them
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09/10/2023
{{c1::Hexokinase}} is in all cells and {{c2::glucokinase}} is induced in the presence of insulin (only in the liver cells and pancreatic beta cells)
Published
09/18/2023
The first step of glycolysis is {{c1::irreversible::reversible or irreversible}}{{c2::Glucose}} + {{c2::ATP}} -> {{c3::G6P}} + {{c3::ADP}} via {{c4…
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09/10/2023
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09/10/2023
The 2nd irreversible step in glycolysis is when F6P is converted into F-1,6-BP by {{c1::PFK1}}
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09/10/2023
The rate limiting step of glycolysis is formation of {{c1::F-1,6-BP}} by {{c1::PFK1}}
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09/10/2023
{{c1::PFK2}} can phosphorylate F6P into F-2,6-BP
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09/10/2023
The 3rd irreversible step of glycolysis is the conversion of {{c1::PEP}} to {{c1::pyruvate}} by {{c2::pyruvate kinase}}
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09/10/2023
All of the energy that our body uses is originally derived from the {{c1::sun}}
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09/10/2023
{{c1::Sun energy}} -> {{c2::glucose from plants (photosynthesis)}} -> {{c3::humans eat it}} -> {{c4::ATP is formed in our cells (cellular res…
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09/10/2023
In the light reactions in photosynthesis, light energy removes an H+ from O2, forming {{c1::ATP}} and {{c1::NADPH}}
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09/13/2023
In the calvin cycle, {{c1::CO2}} + {{c1::NADPH}} + {{c1::ATP}} -> {{c2::Glucose}}
Published
09/10/2023
In the TCA cycle, {{c1::NADH}} and {{c1::FADH2}} are made which are high energy electron carriers used in the electron transport chain to generate {{c…
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09/10/2023
The products of {{c1::photosynthesis}} are the reactants of {{c1::cellular respiration}} and vice versa
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09/10/2023
The body's energy mainly comes from {{c1::carbohydrates}}, {{c1::fats}}, and {{c1::proteins}}, basically in that order
Published
09/18/2023
Ketone bodies are produced by the {{c1::liver mitochondria::organ and cellular compartment}} using Acetyl CoA during pathological states like {{c2::ty…
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09/10/2023
Ketone bodies get converted back into {{c1::Acetyl CoA}} at which point they can enter the mitochondria and produce ATP
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09/10/2023
At 12 hours of fasting, your blood glucose levels are low, so {{c1::glucagon}} is secreted to stimulate {{c2::glycogenolysis}}
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09/10/2023
At 24 hours into fasting, your body runs out of glycogen, so it starts {{c1::gluconeogenesis}} in order to make new glucose molecules from amino acidd…
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09/10/2023
Around 1-3 days into fasting, your body runs out of substrates for gluconeogenesis, so it breaks down {{c1::fatty acids}} into acetyl CoA through beta…
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09/10/2023
Brain cells only use {{c1::glucose}} or {{c1::ketone bodies}} for energy
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09/10/2023
The step with {{c1::HMG-CoA synthase}} is the rate limiting step of ketone synthesis
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09/10/2023
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The 3 ketone bodies are {{c1::acetoacetate}}, {{c2::acetone}}, and {{c3::beta-hydroxybutyrate}}
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09/10/2023
{{c1::Acetone}} is metabolically useless to cells, so it is exhaled from the lungs, giving the breath a sweet smell like in diabetic ketoacidosis …
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09/10/2023
Ketone bodies are acidic molecules that can lower the {{c1::blood pH}}, causing {{c2::metabolic acidosis}}
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09/13/2023
{{c1::Beta-hydroxybutyrate::ketone body}} and {{c1::acetoacetate::ketone body}} can diffuse into the mitochondria of {{c2::peripheral tissues}} where …
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09/10/2023
{{c1::RBCs}} can't use ketone bodies because they don't have mitochondria
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Liver cells don't have {{c1::thioporase}}, so they can't use ketone bodies for energy
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09/10/2023
{{c1::Triglycerides}} are the main storage form of fats
Published
09/13/2023
In fatty acid synthesis, we are trying to make {{c1::palmitoyl-CoA::final product}} from acetyl CoA molecules, and this process occurs in {{c2::liver}…
Published
09/13/2023
Pyruvate from glycolysis moves into the mitochondria where it is converted into acetyl CoA by {{c1::pyruvate dehydrogenase}}
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09/18/2023
Fatty acid synthesis occurs in the {{c1::cytoplasm::cellular organelle}}
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09/10/2023
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NADPH can be made from {{c1::malic enzyme}} during the citrate shuttle or from the {{c1::pentose phosphate pathway }}
Published
09/17/2023
FATTY ACID SYNTHESISAcetyl CoA carboxylase has 3 cofactors{{c1::ATP}}{{c1::Biotin (vitamin B7)}}{{c1::Carbon dioxide}}
Published
09/10/2023
The rate limiting step of fatty acid synthesis is the conversion of {{c2::acetyl CoA}} into {{c2::malonyl CoA}} by {{c1::acetyl CoA carboxylase}}
Published
09/13/2023
Insulin {{c1::removes::removes or adds}} a phosphate group from acetyl CoA carboxylase, {{c2::increasing}} its activity
Published
09/10/2023
Glucagon {{c2::adds}} a phosphate group to acetyl CoA carboxylase, {{c1::decreasing}} its activity
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09/12/2023
{{c1::Citrate}} allosterically {{c2::increases}} the activity of acetyl CoA carboxylase, while {{c1::fatty acids}} allosterically {{c2::inhibits}} it&…
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09/10/2023
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09/10/2023
Per cycle of fatty acid synthesis, we need {{c1::1 acetyl CoA}} -> {{c1::malonyl coA}} and 2 {{c2::NADPH}} molecules
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09/10/2023
Triglycerides are stored in the {{c1::liver}} and {{c1::fat}} cells
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09/13/2023
Insulin binds to insulin receptor which causes {{c1::GLUT4}} to translocate to the cell membrane and allow glucose to move into the cell
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09/10/2023
Insulin activates {{c1::Glucose uptake::glucose}}{{c1::Glycogenesis::glycogen}}{{c1::Glycolysis (when glycogen storage capacity is reached)::glucose v…
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09/13/2023
Insulin inhibits{{c1::Glyogenolysis::glycogen}}{{c1::Gluconeogenesis::glucose}}{{c1::Lipolysis::fats}}{{c1::Proteolysis::protein}}
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09/10/2023
{{c1::Type I diabetes mellitus}} comes from T cells attacking the pancreas due to decreased {{c2::self tolerance}}
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09/10/2023
{{c1::Type 2 diabetes}} is caused by insulin resistance
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09/10/2023
Insulin is administered {{c1::subcutaneously}} because they can be broken down in the GI tract
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09/10/2023
Rapid acting and short acting insulins are used for {{c1::bolus insulin regimen}}
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09/10/2023
Intermediate acting, long acting, and ultra long lasting insulins are used for {{c1::basal insulin regimen}}
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09/13/2023
{{c1::Sliding scale regimen::type of insulin regimen}} is done when a person's glucose levels could fluctuate rapidly
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09/10/2023
{{c1::Basal bolus regimen}} is where basal insulin is used to maintain fasting blood glucose levels and bolus insulin is taken before meals
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09/10/2023
Rapid acting insulins are preferred for treating {{c1::diabetic ketoacidosis}}
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09/13/2023
{{c1::Short acting insulin}} is the only insulin that can be given both subcutaneously and IV
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09/13/2023
The main side effect of insulin therapy is {{c1::hypoglycemia::main one}}, {{c1::hypokalemia}}, and {{c2::lipid dystrophy}}
Published
09/10/2023
Different types of insulinRapid acting: {{c1::aspart}}, {{c1::glulisine}}, {{c1::lispro}}Short acting: {{c2::regular insulin}}Intermediate acting: {{c…
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09/10/2023
Insulins onset of actionRapid acting: {{c1::less than 30 minutes}}Short acting: {{c1::30 minutes}}Intermediate acting: {{c2::between 1 and 2 hours}}Lo…
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09/10/2023
Peak effect time of insulinsRapid acting: {{c2::~1 hour}}Short acting: {{c2::2-3 hours}}Intermediate acting: {{c2::4 hours}}Long acting: {{c1::none}}U…
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09/10/2023
After you eat, when glucose is broken down into ATP, the K+ channels {{c1::close}}, {{c1::increasing}} the K+ concentration in the cell causing {{c2::…
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09/10/2023
Sulfonylureas cause K+ channels to close, {{c1::increasing}} insulin production. They also {{c2::decrease}} gluconeogenesis and {{c2::increase}} perip…
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09/10/2023
{{c1::Meglitinides}} work the same way as sulfonylureas, but they are more fast acting
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09/18/2023
{{c1::Incretins::category of hormones}} stimulate insulin release after a meal
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09/10/2023
{{c1::DPP-4 inhibitors}} inhibit DPP-4 from inactivating GLP-1, which allows GLP-1 to exert its effects for longer
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09/14/2023
Sulfonylureas:Names; {{c1::glyburide}}, {{c1::glipizide}}, {{c1::glimepiride}}Mechanism: {{c4::block ATP-sensitive K+ channel}}Side effects: {{c2::wei…
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09/10/2023
Meglitinides:Names: {{c1::end in -glinide}}Mechanism: {{c2::block K+ pump}}Side effects; {{c3::weight gain}}, {{c3::hypoglycemia}}
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09/10/2023
GLP-1 receptor agonistsNames: {{c3::end in -tide}}Mechanism: {{c1::increase insulin secretion}} and {{c1::decrease glucagon release}}Side effects: {{c…
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09/13/2023
DPP-4 inhibitorsName: {{c1::end in -gliptin}}Mechanism: {{c2::inhibit DPP-4 from breaking down GLP-1}}Side effects: {{c3::headache}}, {{c3::nasopharyn…
Published
09/25/2023
OTC Deficiency in the Urea Cycle leads to increased levels of {{c1::Carbamoyl Phosphate}}
Status
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