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by: Mikaela Maldonado

BMSWeek13Notes.pdf BMS 260

Mikaela Maldonado
GPA 4.0

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About this Document

All rights go to Dr. RV Anthony but all work is my own
Biomedical Sciences
Dr. Russell Anthony
Class Notes
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This 5 page Class Notes was uploaded by Mikaela Maldonado on Saturday April 23, 2016. The Class Notes belongs to BMS 260 at Colorado State University taught by Dr. Russell Anthony in Spring 2016. Since its upload, it has received 16 views. For similar materials see Biomedical Sciences in Biomedical Sciences at Colorado State University.

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Date Created: 04/23/16
Secretions into the lumen of the stomach  Gastric pepsin  Endoprotease  Pancreatic  Endoprotease  Trypsin  Chymotrypsin  Carboxypeptidase  Exoprotease  Brush Border enzymes  Microvilli lining the digestive tract  Amino peptidase  Carboxypeptidase  Dipeptidase  Amino acid absorption  Na+ co transport mechanisms  Apical (microvillar) surface  Na+ independent transport  Basolateral  More detrimental side if it malfunctions  Peptide transport  H+ cotransport of di or tripeptides  Limited whole protein absorption  M Cells – special enterocytes  Carbohydrates  Consumed as disaccharides or poly saccharides  Sucrose, lactose, maltose, starch, glycogen, etc.  Has to be absorbed as monosaccharides in the intestines  Starch or pancreatic amylase  Starch or glycogen  Maltose, maltotriose, and oligosaccharides  Some oligosaccharides are Alpha- limit dextrins because they contain a branch point  Have to get down to monosaccharides but amylase doesn’t do that …  Brush border enzymes come into place here  Glucose and galactose  Transported by SGLT1 on the apical surface  Na+ dependent  Fructose  5 carbon sugar  transported by GLUT5  facilitated transport mechanism  basolateral  transport by GLUT 2  lactase  breaks down lactose to galactose + glucose  Maltase  Breaks down maltose to glucose x2  Sucrose – Isomaltase  Sucrose to glucose + fructose  Maltotriose and alpha limit dextrins to glucose  Lactose Deficiency  Deficiency in lactose derived glucose/galactose absorption  Colonic digestion of lactose -> H2 and CO2  Lipids  Dietary lipids include triglycerids, di and mono glycerids, phospholipids and cholesterol  Bile salts – help with emulsification  Pancreatic lipase  Colipase  Lipid droplet – micelle  Cholesterol, free fatty acids and monoglycerides will diffuse across membrane  Enterocyte rebuilds triglycerides  Coupled with apolipoproteins (liver makes these)  Combine the tri and mono glycerides to form chylomicrons or very low density lipoproteins (VLDL)  Glucose Storage  Blood has glucose and amino acid that are taken up by the muscle and stored as glycogen  Adipocytes  Triglycerides in the blood are converted to fatty acids and monoglycerides through lipoprotein lipase  Glucose is taken up and alpha glycerol phosphate and fatty acids (from the blood) form triglycerides and then are stored as glycerol  Fat cells – hormone sensitive lipase  Catecholamines, glucagon, cortisol stimulates hormone sensitive lipase activity  Liver  Glucose is taken in and participates in the Krebs Cycle  Nutrient Metabolism during the absorptive period  Energy is provided by carbs in meals  Net uptake of glucose by liver  Carbs stored as glycogen in liver and muscle but most carbs and fast are stored as fat in adipose tissue  Synthesis of body proteins, but some amino acids in dietary protein are used for energy or converted to fat  Absorptive phase is anabolic and uses insulin  Post absorptive phase is catabolic  Nutrient metabolism during post absorptive period  Glycogen, fat, and protein syntheses are curtailed and net breakdown occurs  Glucose is formed in the liver both from glycogen stored there and by glycogenesis from lactate in blood, pyruvate, glycerol, and amino acids. Kidneys will perform glycogenesis during a fast  Glucose is produced in the liver and kidneys is release in to the blood but its use for energy is greatly reduced in muscle  Lipolysis releases adipose-tissue fatty acids into the blood, and oxidation of these fatty acids by most cells and of ketones produced from them by the liver provides most of the body’s energy supply  The brain continues to use glucose by also starts using ketones as they build up in the blood  Concentration of cellular energy (ATP)  Mitochondria  Krebs or TCA cycle  Begins with acetate (2 carbons)  Oxidative phosphorylation – electron transport chain  Glycolysis – metabolism of glucose  Beta- oxidation – metabolism of fatty acids, and will eventually give rise to acetate  Gluconeogenesis – generation of new glucose (liver)  Insulin effects  Absorptive phase (increase plasma insulin)  Muscle  Increase glucose uptake, glycogen, synthesis, amino acid uptake, and net protein synthesis  Adipocytes  Increase glucose uptake and net triglyceride synthesis  Liver  Increase glucose uptake, net triglyceride synthesis, no ketone synthesis  Post absorptive phase (decrease plasma insulin) opposite of above Reproduction  Hypothalamic – pituitary – gonadal axis  Hypothalamus releases GnRH through the hypothalamo-pituitary portal vessels  Activates the anterior pituitary to secrete FSH and LF which go to the gonads which secrete sex hormones that go to gametogenesis and then produce action on sex organs  Stages of control of reproductive function  During the initial stage (fetal life to the end of the first year), GnRH, the gonadotropins, and gonadal sex hormones are secreted as relatively high levels  Infancy to puberty, secretion rate of these hormones are very low and reproductive function is quiescent  Beginning at puberty, hormonal secretion rates increase and show large cyclical variations in women during the menstrual cycle. Allows for active reproduction  Reproductive function diminishes late in life, largely because the gonads become less responsive to the gonadotropins  Sex determination  X and Y chromosomes determine sex  Phenotypic sex is dependent on genetic sex, gonadogenesis, formation and maturation of accessory reproductive organs  Start  Two undifferentiated gonads  Two pairs of undifferentiated ducts  Mullerian or Wolffian ducts  Urogenital sinus  Genital tubercle  Vestibular folds  Embryo  Epithelial and yolk sac cells migrate to the germinal ridge  Yolk sac cells give rise to sex cords and what will become the gonads  More specifically will give rise to the seminiferous vesicles in the testes  Testes will produce testosterone as well as Mullerian inhibiting substances which will differentiate the duct systems so that they go in the right direction  Epithelial cells will give rise to the ovaries  Rudimentary gonad  Outer layer (cortex)-> ovary  Inner layer (medulla) -> gives rise to the testes  Differentiation of the gonads  Seventh week of fetal development of the SRY gene on the y chromosome that leads to the development of testes in male  Guest lecture:  Started in a lab in Tulane  First generation student  Brain differentiation all the way to gut function  Then went to U of CA SB  Leverage – rats and steroids experiments in brain and behavior studies  Married and moved to MIT  Aromatase  Sexual differentiation studies  Converts testosterone into estrogens  Shriver Center  Mental hospital to try and understand the neurology  Lorenzo’s Oil  Hypothalamic pituitary nucleus region  3-fold denser vasculature as compared to any other region of the brain  tied to obesity, depression, cardiovascular health  found to be able to to be manipulated  window to changing brain function  biomedical engineering  put live tissue into a dish and then allow to see live function of the cells in the dish


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