NPB101: Endocrine System Lec 1 Part 2

Primary Energy Storage Molecules

stored as fats or glycogen

Glycogen

stored glucose

We transform ___ into ATP or release energy from storage molecules, this is ____ (anabolism/catabolism)

nutrients, catabolism: because its the breakdown of stored nutrients (i.e. fasting & exercising)

T/F: When we have excess nutrients we store them

True, when we have excess nutrients we store them this would be anabolism as we use these store excess: liver-glycogen that gets broken down into smpler ones (glc) releases into bloodstream for fasting like CATABOLISM, muscles: glycogen for energy during activity

What happens/what do we do with our stored nutrients?

When nutrient levels drop in the blood we use these fuel stores to maintain glucose and energy levels (Fuel Homeostasis) (primarily catabolism)

Catabolism (cutting/breaking down)

• resting

• fasting —→ break down stored fats

• break down fats so you will not be eating while doing this

• exercise —→ you used stored fats (reserves)

Anabolism (Add)

• using energy to build, storing, and repair tissues —→ muscles and proteins

• state of growth (eating)

• eating

Fed or Absorptive State

• when we store nutrients after eating (anabolism)

• high blood sugar also occurs due to recent food intake

Fats are stored in ____ tissue

adipose

Carbohydrates are stored in ___ skeletal muscle & in the ___

resting, liver

Rested Fasting State (not eating) POSTABSORPITIVE

when we break down our energy stores mainly at adipose tissue and also at the liver (Catabolism) NOT PROTEINS (only when we are deeply starved where is weakend our muscles)

When you are exercising are you increasing you’re rate of catabolism or anabolism?

Catabolism because when you are exercising it breaks down stored fats to releases energy, fats are energy rich molecules

When you are exercising are you increasing you’re rate of catabolism or anabolism? Explain the other side

Not anabolism because it takes up energy to build something up something like proteins and muscles

Pancreatic Hormone

T/F: The majority of the cells inside the pancreas are involved in gastrointestinal function

True

Pancreas

Contains Endocrine & Exocrine

Endocrine

Exocrine cells

pushes secretion out “exo” of pancrease and then into small intestine

Islets of Langerhans

• doesn’t produce secretions into GI tract it, but does produce endocrine cells of the pancreas including:

  • ß (beta) cells

  • α (alpha) cells

  • ∂ (delta) cells

ß (beta) cells

produces Insulin

Insulin

allows cells in your body absorbs glucose when blood sugar is high

α (alpha) cell

produces glucagon(breakdown of glycogen→glucose) in pancreas and then released into bloodstream where it targets organs like liver

Glucagon

at liver is signals liver cells to break down stored glycogen into glucose (catabolism) and release it to raise bloodstream levels

∂ (delta) cells

produce pancreatic somatostatin (shuts production off at certain things/regulatory hormone)

T/F: Insulin is in the Postabsorpative state

False, Insulin is released in the absorptive state because after you eat your blood glucose levels rise triggering your beta cells in the pancreas to release insulin its which helps cells absorb glucose and its also in absorptive state because this occurs right after we eat (Humoral regulation)

Humoral Regulation

During high blood glucose, like after eating, the blood acts as a humoral trigger that stimulates beta cells to release insulin.

During low blood glucose, alpha cells detect the drop and release glucagon, which signals the liver to break down stored glycogen into glucose to raise blood sugar levels.

Parasympathetic (Peace) —→ Rest & Digest/ Absorptive State

anabolism: this is adding nutrients to storage by digesting the food

Sympathetic (Stress) —→ Fight-or-Flight

catabolism: because you need energy fast when going through this response

releases epinephrine as this is released by adrenal medulla to break down glycogen

Incretin —→ Anticipatory (anticipates)

occurs before blood glucose levels rise

IGF

insulin like growth factor

GLUT 4

• is used when blood glucose levels rise after we eat

• can increase glucose uptake through this at the muscle, adipose tissue and heart

T/F: GLU4 is glucose dependent

True, GLU4 is glucose dependent because it responds to insulin & increases glucose uptake

___ is the main storage molecule of glucose in our cells

Glycogen

Carbohydrate

GNG (Gluconeogenesis)

• occurs during fasting/exercise —→ catabolism (breaking down molecules)

• process of creating new glucose from nonglycogen/noncarbohydrate sources, so it uses glycerol (from the breakdown of)—→ fats, a.a. from the breakdown of—→ proteins, lactate produced by—→ muscles, liver takes these precursors (glycerol,aa, lactate) & releases it into bloodstream

• provides glucose when blood sugar levels are low

Glycogenesis

Store glucose as glycogen —→ ANABOLISM

Glycogenolysis

break down(lysis) of glycogen

During Carbohydrate metabolism:

• Reduce glycogenolysis(breakdown of fats) because you want to store fats not break them

• reduce gluconeogenesis (don’t need to make new sugar cus you just ate)

• Insulin decreases the blood glucose levels as insulin allows glucose to be absorbed but not all of it as it promotes storage as well (regulate)

Fat Metabolism

• storing fats (lipogenesis) when you have extra energy —→ GLUT4 (glc dependent) responds to insulin as insulin allows cells to absorb & store fats after meal

• decreases lipolysis

• insulin lowers fatty acids in the blood and promotes fat storage by keeping them stored as adipocytes

Lipogenesis

create triglycerides from glucose or other sources for storage

• eat → blood level high → insulin released → allows cells to absorb glc

• if more glucose than needed it’ll be converted to fatty acids

  • F.A. + glycerol → triglyceride →stored in adipocytes

Adipose (Adipocyte)

fat cell

Lipolysis

breakdown of triglycerides into f.a. + glycerol (lysis→break)

Fatty Acids

stored inside adipocytes (fat cells) and stores as part of triglycerides bc f.a. + glycerol= triglycerides

• after eating → insulin allows absorption to occur → store some (↑ lipogenesis) → bc not all f.a. will be released into blood (↓ lipolysis) then as some are being stored with glycerol → creating triglycerides → stored as adipocyte

Protein Metabolism

• a.a. into tissue → promote protein synthesis & inhibit protein breakdown

  • eat protein → gets digested → become a.a. → a.a. enter the blood

• Insulin promotes protein synthesis by helping cells take in a.a. → build proteins → stops the body from breaking proteins down

Absorptive effects are generally (induced/caused)___ by an (inc/dec)___ of insulin

induced, increase

Post-absorptive effects are generally (induced/caused)___ by an (inc/dec)___ of insulin

caused, decrease

Glucagons goal is to ____(increase/decrease) levels of blood glucose

increase: this is done by the alpha cells that release glucagon when it detects the drop in blood glucose which then signals liver to release stored glycogen

when glucose levels (drop/increase)___ the α-cell releases ___ (insulin/glucagon)

drop, glucagon

Carbohydrate Metabolism

• Glycogenolysis

• Inhibition of glycogenesis

• Hepatic gluconeogenesis → make glucose

• Hepatic glucose release

T/F: In carbohydrate metabolism it is allowing glycogenesis

False, in carbohydrate metabolism it is inhibiting glycogenesis because we want to not store only just absorb not store

Fat Metabolism

• Lipolysis

• Inhibition of fat synthesis

• Hepatic fatty acid release

T/F: In fat metabolism is its the inhibition of fat synthesis

True in fat metabolism it inhibits fat synthesis

T/F: Protein Metabolism does not have much effect on protein breakdown

True

T/F: Glucagon has an affect on protein breakdown

False it does not have effect, its typically cortisol breaking down protein

T/F: Gluconeogenesis is stimulated by glucagon

True because glucagon is from storage and to glucose and gluconeogenesis does the storing

Hyperglycemia

• characterized by chronic high blood glucose levels

Type I → Insulin Dependent

due to insufficient insulin secretion

Type II → Insulin Independent

due to lack of effect of insulin

Diabetes Mellitus

• characterized by chronic high blood glucose levels

• Type I → Insulin Dependent

  • 5% of diabetes are this type

• Type II → Insulin Independent

  • 95% of diabetes are this type

  • don’t produce storage molecules

Type I Diabetes Mellitus

• ß cells are progressively destroyed

• Glucose is unable to enter resting muscle or adipose cells

  • fatty acid → ketone bodies that produce ketoacidosis

• Increased glucagon levels stimulate glycogenolysis in liver

Why do Increased glucagon levels stimulate glycogenolysis in liver?

1. There is an increase in glucagon levels

   • your body thinks your blood glucose levels are low, but they are actually high, but your body doesn’t know that because the cells can’t absorb

2. So because your cells cant absorb no insulin is being produced in pancreas and insulin usually allows the absorption

   • so here with lack of insulin your body thinks its starving even while blood sugar high

3. So your α cells keep releasing glucagon and because glucagons job is to raise blood glucose it signals the liver to break down the stored glycogen

   • glycogen→ glucose

4. The release of glucose into the blood is called glycogenolysis

Consequences of Type I Diabetes Mellitus

Acute consequences:

• Excess urination

• Excess thirst

• Muscle wasting

• Muscle weakness

• Metabolic acidosis (Ketosis)

Chronic complications involve:

• Degenerative disorders of blood vessels and nervous system

  • Cant feel/ detect things → neurons destroyed

• Increased risk of kidney failer

• Account for the shorter life expectancy of diabetes

• Don’t grow very tall

Consequences of Type II Diabetes Mellitus

Associated with:

• Over secrete insulin → Obesity

• Lots of fat food → High plasma triglycerides

• High plasma glucose

• High blood pressure

• Decreased insulin sensitivity

  • tissue no longer responding to insulin

Treatments:

• Thiazolidinediones (TZD): increases insulin sensitivity of tissues

• Metformin: Decreases hepatic (liver tissues) glucose release

• Easiest Treatment: diet and increased activity