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Cortisol hormone Cortisol inhibits glucose uptake, stimulates protein degradation, promotes both lipolysis & gluconeogenesis Gluconeogenesis: conversion.

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Presentation on theme: "Cortisol hormone Cortisol inhibits glucose uptake, stimulates protein degradation, promotes both lipolysis & gluconeogenesis Gluconeogenesis: conversion."— Presentation transcript:

1 Cortisol hormone Cortisol inhibits glucose uptake, stimulates protein degradation, promotes both lipolysis & gluconeogenesis Gluconeogenesis: conversion of amino acids into carbohydrates at liver

2 Control over cortisol ACTH from anterior pituitary stimulates cortisol secretion Negative feedback from cortisol inhibits hypothalamus and anterior pituitary

3 Cushing’s syndrome Excessive cortisol - often due to tumor at pituitary or adrenal gl. Excessive gluconeogenesis

4 Cortisone injections:
Patients take cortisone (converts to cortisol) for anti-inflammatory effects (allergies, arthritis, trauma). Immune system is suppressed.

5 Chronic (continual) release of stress hormones
Stress responses: SNS effects (vasoconstriction, anxiety) Fat, sugar blood levels (diabetes, arterioscl) Fluid retained, BP (hyperten, heart disease) Immune system fxn, sexual fxn, digestion all decrease (infertility, irritable bowel, ulcers, vomiting)

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7 Adrenal gland: sex hormones
DHEA from adrenal cortex is a source of ‘opposite’ sex hormone in men and women ACTH controls adrenal androgen secretion DHEA testosterone in women

8 Adrenal medulla Functions as a modified postganglionic neuron of the sympathetic NS. It stores and secretes epinephrine and norepinephrine In addition to FOF responses, stimulates glucagon secretion and inhibits insulin secretion.

9 Pancreas: endocrine hormones
Alpha cells release glucagon Beta cells release insulin Islets of Langerhans

10 Insulin:storage and anabolism
Insulin signals to fat and other tissues to take up glucose (GLUTs). Prevents the mobilization of fat. Liver takes up fatty acids, makes glycogen GH, cortisol, epinephrine, and glucagon inhibit insulin.

11 Metabolism Anabolism – building large molecules from smaller ones, requiring energy Promoted by insulin, GH Catabolism – breaking down large molecules into smaller ones. Energy is released Promoted by glucogon, cortisol

12 How the body controls metabolism
Nutrients must be stored then released between meals. The brain needs a constant supply of glucose Most conversion of molecules occurs in the liver. Nutrients that cannot be formed this way are “essential” nutrients and must come from diet.

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14 Storing energy in the body
Excess glucose glycogen in liver and muscles (or adipose when there is much glycogen) Excess fatty acids triglycerides, in adipose Excess amino acids triglycerides, in adipose Glycogen (pink) in liver cells

15 Blood glucose levels Glucose levels are consistent over the day, range about 10-15%, through action of insulin and glucagon Between meals, body cells can burn fatty acids to spare glucose for the brain. Blood glucose Insulin

16 Blood glucose levels and glycemic index
With simple carbs (high glycemic index) glucose absorbed to blood rapidly - insulin spike that follows is large. Glucose reduced in blood

17 Blood glucose levels and glycemic index
With simple carbs (high glycemic index) glucose absorbed to blood rapidly - insulin spike that follows is large. Glucose reduced in blood With lower glucose levels, may crave food again

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19 What is diabetes? Inadequate insulin action = diabetes mellitus (hyperglycemia) Type I “juvenile diabetes” - body cannot produce insulin – autoimmune disease Type II “adult diabetes” too little insulin made, or target cells are insulin resistant

20 Apple vs. Pear

21 Adipose and insulin resistance
Diabetes, insulin resistance (IR) is associated with obesity, lack of exercise When storage at fat cells is exceeded, free fatty acids (FA) in blood increase

22 Adipose and insulin resistance
High FA may cause muscle and adipose to diminish their response to insulin (IR) Insulin less able to clear glucose from blood, still helps store fat.

23 Are there mutations that promote obesity?
“Genome-wide studies have led to the discovery of nine loci (Mendelian) and 58 loci (polygenic) associated with obesity. These loci explain a small fraction of the heritability for obesity and many genes remain to be discovered”

24 Appetite-related hormones (just for your own interest...not for exam)
Ghrelin – released at stomach, duodenum when absence of food. Stimulates appetite. Peptide YY released by ileum, colon in response to presence of food. Inhibits appetite. (eating protein can boost PYY) Leptin – released by adipose, inhibits appetite. (Obese people can have decreased response to it, still have lower levels when wt. lost) Mouse w/ leptin mutation

25 “Indifferent” ducts of embryo
Y chromosome present Y chromosome absent Male Female uterus ovary vagina penis testis

26 Biology of gender Sex chromosomes determine gonadal sex (testis-determining factor) Phenotypic sex is depends on development of external genitalia w/hormone

27 Differentiation of genitalia depends on whether testosterone is present
At 7 weeks Undifferentiated genitalia

28 Intersex individuals experience opposite sex hormones during early development or are insensitive to normal hormones. Some examples: Androgen insensitivity Lack of enzyme for testosterone production Congenital adrenal hyperplasia (enzyme missing to produce cortisol, aldosterone. Steroids converted to androgens instead.)

29 Male reproductive anatomy

30 Descent of the testes During fetal development, testes move from abdomen into scrotum Inguinal area is a common spot for hernias (intestine pokes through abdominal wall) The scrotum provides a cool area optimal for spermatogenesis


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