Bolded Question

What substances are found in gastric secretions? What is the role of each secretion? What cells produce each of these secretions? What regulates parietal cells and HCl secretion? Describe HCl secretion.

The substances that are found in the secretions are the mucous neck, parietal cells and chief cell. The mucous neck cell produces mucous to protect against the low pH. The parietal cells produce HCl to sterile, denature, activate pepsinogen and Intrinsic factor that binds with vitamins B12 for RBC production). Chief cells produce enzymes that are gastric lipase to break down the 3 branches which are the Triglycerides. Pepsinogen (inactive) when HCL is around it’ll be pepsin to break down protein.

What are the functions of the liver? What are bilirubin, conjugated bilirubin, and stercobilin? What is jaundice? What is deamination – how does it relate to BUN? What makes up bile? Describe blood flow through the liver. What is enterohepatic circulation?

• The functions of the liver are bile production, carb, lipids, protein metabolism, production of plasma protein such as albumin and clotting protein, and detoxification for drugs and alcohol. It’s RBS recycling. 

• Bilirubin are RBC lysis (hemolysis), liver production, in newborns. Conjugated bilirubin is part of bile for gallstone and pancreatic cancer, stercobilin is a brown bile pigment that serves as the final breakdown product of hemoglobin catabolism. Jaundice is yellowing of skin, sclera, and mucous membranes. Deamination is the process that removes an amino group, and if the body cannot store excess amino acid when eating more protein than you need, or during fasting/starvation, amino acids are broken down to yield energy. Removing the amino group releases ammonia, which is highly toxic to cells. The remaining carbon skeleton is converted into energy, glucose, or fat. It’s related to BUN because this lab test will help measure the amount of nitrogen stored in the form of urea circulating in the blood. 

• Bile is a digestive fluid produced by the liver that helps emulsify and absorb fats and these are made up of water, bile salts, phospholipids, cholesterol, bilirubin, and electrolytes. Blood flows through the liver by the hepatic artery (O2 rich) and hepatic portal vein (O2 poor) mix with the haptic sinusoids to the hepatocytes to extract O2, nutrients to store, add nutrients in the fasting state, detoxify and recycle RBC’s plus the Kupffer Cell is the phagocytes in liver. 

• Enterohepatic circulation is the eyeclying loop of substances between the liver, the small intestine (duodenum), and the portal bloodstream. 

14. Trace the breakdown and absorption of each of the macromolecules include: enzymes involved, specific locations, and mode(s) of absorption into the gut epithelium and transport into the blood stream. 

• Carbs→ salivary amylase→ no gastric → pancreatic amylase → disaccharides, trisaccharides → sucrase, lactose, maltase

• Proteins → no salivary → pepsin active via HCl → Eletase carboxypeptidase trypsin chymotrypsin → dipeptidase → dipeptidase 

• Lipids → lingual lipase (active in stomach) → Gastric lipase → pancreatic lipase → monoglyceride, 2 fatty acids → no brush border enzyme 

• Nucleic acids → no salivary → no gastric → nuclease ( RNA, DNA) → nucleotides → phosphatidase, nucleosidase

Describe the stimulus, source, target, and effect of the hormones CCK , secretin, gastrin.

• CCK: Stimulus: food in duodenum → Sensor, CC: in the duodenum → secreted → CCK → Effortor: Gallbladder release bile for food breakdown, Pancreas release pancreatic enzyme to break down food. This is negative feedback. 

• Secretin: Stulmus: Acid Chyme → senor, control center: duodenum → secrete → SECRETIN → stimulates → Effector: Pancreas to release NaHCO3 → increase pH (Alkaline chyme). This is negative feedback. 

• Gastrin: Stimulus: food in the stomach → sensor/control center: stomach special cell called G cells – will stimulate/ secrete → GASTRIN → Effector: stomach to increase motility and secretion → food break down. This is negative feedback. 

Distinguish between micelles and chylomicrons.

• The difference between micelle and chylomicrons differ in their composition, size, location and function. 

• Micelles are made of bile salts, fatty acids, etc contain no proteins, the size is very small, located in the lumen of the small intestine, and they are digested lipids produced through the watery environment of the gut enterocytes for absorption. 

• Chylomicrons are particles with a central core of triglycerides, the size is much larger, located inside the intestinal epithelial cells and secreted into the lymphatic system before entering the bloodstream. They transport newly dietary triglycerides and cholesterol from the intestine to peripheral tissues. 

Specifically, where does the electron transport chain take place in the cell? What is the main purpose of this stage? Does this stage require oxygen? Describe the steps of chemiosmosis.

• The ETC takes place in the inner mitochondrial membrane. The main purpose of this is transferring high energy electrons from NADH and FADH2 through the protein to generate  H+ gradients across the membrane, which will drive the production of a large amount of ATP. Yes, this required oxygen acts as the final electron acceptor at the end of the chain. 

• Chemiosmosis

  • Step 1: NADH + H+ & FADH will each release 2 H atoms → 2 e’s, 2 H+

  • Step 2: 2 e’s are shuttled down to the cytochromes → redox reaction that release energy. 

  • Step 3: Energy released is used 2 pump H+ into the intermembrane space → creates an [H+] gradient. 

  • Step 4: H+ diffuses from high [ ] to low [ ] through ATP synthase → energy released 

  • Step 5:  energy released used to combine ADP + P to make ATP 

  • Step 6: Oxygen receive 2 e- (low energy) & combine with 2 H+ → make H20 

How are fats transported throughout the body? What are VLDL’s, HDL’s and LDL’s? What are apoproteins, lipoproteins, and lipoprotein lipase? Distinguish between Apo E, Apo B100,Apo A1. 

• Fats are transported throughout the body by lipoproteins so they can travel through the bloodstream. 

• VLDL: Very Low Density Lipoprotein 

  • High production with high fat diet

  • Content: have TG’s & Cholesterol 

  • Role: adipose and muscle tissues to deliver TG 

  • Receptor: Apo E: high affinity Apo B100: low affinity 

• HDL: High Density Lipoprotein

  • Produced by the liver

  • Receptor: Apo 1: high affinity 

  • Role: pick up cholesterol from peripheral tissues 

  • HDL: “Good” cholesterol 

• LDL: Low Density Lipoprotein 

  • Only the Apo B100 receptor will have a long life span in the blood. 

  • Content: cholesterol accumulates along the tunica intima of arteries. 

  • LDL is called the “bad” cholesterol. It'll lead to atherosclerosis because the cholesterol will build up to the tissue. 

• Apo E helps the liver recognize and take up remnants, Apo B100 helps LDL blind the LDL receptor on cell to provide structural support for VLDL, Apo 1 activates lipoprotein lipase allowing triglycerides to be broken down. 

Compare and contrast the absorptive and postabsorptive states. What hormones are involved to regulate these states?

• Absorptive states store glycogen synthesis, TG synthesis, and Protein synthesis. The hormone that is involved to regulate this state is insulin. 

• Post-Absorptive: are glycogenolysis, production of ketones bodies → lipolysis, protein catabolism → gluconeogenesis. Hormones that is involved to regulate this state is glucagon, epi, and cortisol (prolonged fasting) 

Diagram the feedback loops for both insulin and glucagon.

• Insulin: (Fed state) Stimulus: High blood glucose → sensory, CC: B cells –INSULIN secreted → increased GLut and Glycogenesis (storage) → Effector: muscle, liver → low blood glucose. 

• Glucagon: (Fasting state) stimulus: low blood glucose → alpha cell – glucagon secreted → Effector: liver to breakdown glycogenolysis and gluconeogenesis → high blood glucose. 

What problems are associated with fat catabolism? How does this relate to diabetes mellitus and long term starvation? What are ketone bodies? What is the condition known as ketoacidosis?

• The problem with fat catabolism is the dangerous acid accumulation when it happens too fast or without enough insulin. It’s related to diabetes mellitus because the body lacks insulin, cells cannot absorb glucose from the blood. It’ll make the liver think of a false starvation state to flood the bloodstream with high blood sugar, and rapidly down fat to compensate. This will lead to Diabetic Ketoacidosis. Long term starvation when someone goes without food or carbohydrates for a long period of time. The body switches to fat catabolism as a survival to produce a level of ketones for the body to balance leading to starvation ketoacidosis. Ketone bodies are water-soluble acid byproducts made by the liver. Ketoacidosis is a life-threatening metabolic state where excessive amounts of ketone bodies build in the blood, making it dangerously acidic.