DOC PREVIEW
UCSD BICD 150 - Set 7
Type Lecture Note
Pages 8

This preview shows page 1-2-3 out of 8 pages.

Save
View full document
Premium Document
Do you want full access? Go Premium and unlock all 8 pages.
Access to all documents
Download any document
Ad free experience

Unformatted text preview:

BICD 150 Sp 14 Fortes 7 5 13 14 1 of 7 Lecture 13 Review of embryonic sexual development In this figure Anti Mullerian Hormone AMH is referred to as MIF The prostate and the male external genitalia require DHT as well as testosterone to develop The embryo contains bi potential gonads that begin to differentiate between 7 8 weeks The cortex of these gonads will develop into ovaries or the medulla will develop into testes if there is a functional SRY gene on a Y chromosome Wollfian ducts require testosterone to develop and degenerate in female embryos Testosterone also allows for the descent of the testes into the scrotum via the inguinal canal before birth Page 1 of 7 Testes have Leydig cells get stimulated by LH or placental hCG to secrete T 5 a Reductase will convert some of this into DHT T will stimulate the development of the wollfian ducts and DHT will cause male differentiation of the penis and scrotum Sertoli cells will secrete AMH to cause degeneration of the mullerian ducts Disorders of embryonic sexual development Mutated nonfunctional aromatase Low no production of female hormones in the female embryo Androgens including T will increase since it is not being converted to E2 There may be development of wollfian ducts since T is high Mutated nonfunctional 5 a Reductase No conversion of T into DHT External genitalia will develop as female There will also be little to no growth of the prostate Wollfian ducts will still develop into male accessory structures since there is still T being secreted by the testes Mullerian ducts degenerate due to the secretion of AMH o There are drugs that can be prescribed that inhibit 5 a Reductase These are useful to treat hypertrophy or enlargement of the prostate in aging males since DHT is what stimulates its growth Non functional androgen receptors Testicular Feminization Testes will still be present due to the SRY gene Sertoli cells secrete AMH to degenerate the mullerian ducts Leydig cells secrete T which can be converted to DHT but there will not be any effects due to the lack of receptors Wollfian ducts also degenerate due to the lack of effects of T Female external genitalia due to lack of DHTs effects Hormonal Effects during Puberty GnRH starts pulsing to initiate puberty and the secretion of FSH and LH These hormones stimulate the gonads to greatly increase secretion of E2 or T The age of onset of puberty has been decreasing This has been attributed to better nutrition However it is now believed that childhood obesity is contributing to earlier puberty In 1994 a hormone secreted by adipocytes was discovered called Leptin It was discovered that mutant rats mice that could not produce the hormone were extremely obese Leptin is an important appetite inhibitor The mice also did not undergo puberty It is believed that Leptin is an important signal to begin puberty Obese children have larger and more numerous adipocytes and more leptin is secreted This could cause earlier puberty Female Earlier growth spurt than boys Development of breasts Development of female pattern pubic hair inverted triangle Axillary hair Redistribution of fat under the effect of E2 female hourglass figure Page 2 of 7 Menstruation Acne Male Deepening of voice Development of facial hair Growth of penis and testes Growth spurt Broadening of shoulders Increase in muscle mass Acne Hormonal changes after puberty Males remain fertile throughout their lives after puberty However the ability of the testes to secrete T and DHT decreases with age This generally causes an increase in FSH and LH T and E2 inhibit bone resoprtion Low levels of T E2 will cause an increase in bone resorption that can lead to osteoporosis this is more common in again females however Females go through menopause generally in their early 50s All ovarian follicles have been ovulated or have died This causes an enormous drop in estrogens that normally come from the ovaries Some E2 is still made by peripheral conversion of androgens from the adrenal cortex via aromatase but it is greatly reduced No longer menstruate Increased osteoporosis Hot flushes flashes End of Reproduction Lecture let out 25 minutes early today Enjoy the great weather Page 3 of 7 BICD 150 Sp 14 Fortes 7 5 15 14 4 of 7 Lecture 14 Pancreatic hormones The pancreas has both exocrine and endocrine function It secretes bicarbonate rich pancreatic juice to neutralize stomach acid as well as inactive digestive enzymes known as Zymogens into ducts that lead into the small intestine in an exocrine fashion As an endocrine organ the pancreas secretes several hormones from a variety of cell types called Islets of Langerhans Alpha cells 25 of Islet volume Secrete Glucagon Beta cells 55 of Islet volume Secrete Insulin and C Peptide Delta cells 10 of Islet volume Secrete Somatostatin inhibits mainly glucagon secretion as well as insulin to an extent Epsilon cells 3 of Islet volume Secrete Ghrelin hormone mainly secreted by the stomach that is known to increase appetite Insulin and Glucagon regulate metabolism and blood glucose levels in an antagonistic yin yang fashion Insulin Hormone of the fed state that makes you fat Eating and absorbing nutrients will stimulate its secretion Promotes Anabolism Increase Lipogenesis Increase Protein synthesis Glycogen synthesis Increase carbohydrate metabolism Is a growth factor has mitogenic effects Page 4 of 7 Glucagon Hormone of the fasted state Increases availability of substrates to be used for energy when you haven t eaten food is low Catabolism Increase Lipolysis Increase Glycogenolysis Increase Gluconeogenesis Increase protein breakdown in extreme cases The secretion of insulin and glucagon are both extremely dependent on blood glucose levels High blood glucose stimulates insulin and inhibits glucagon Low blood glucose stimulates glucagon and inhibits insulin Insulin A protein secreted by the beta cells Proteins that are destined to be exported from cells are synthesized as larger precursors in the rough ER where they are folded From there vesicles containing the precursor proteins are sent to and further processed in the Golgi Vesicles containing the final form of the protein are then exocytosed upon receiving the appropriate signal Synthesized as Pro Insulin and cleaved into Insulin and C Peptide by proteases C Peptide has no activity but since Insulin has a very short half life high turnover via the liver C Peptide can be measured to get an idea of how much insulin is being secreted Stimulation of


View Full Document

UCSD BICD 150 - Set 7

Type: Lecture Note
Pages: 8
Download Set 7
Our administrator received your request to download this document. We will send you the file to your email shortly.
Loading Unlocking...
Login

Join to view Set 7 and access 3M+ class-specific study document.

or
We will never post anything without your permission.
Don't have an account?
Sign Up

Join to view Set 7 and access 3M+ class-specific study document.

or

By creating an account you agree to our Privacy Policy and Terms Of Use

Already a member?