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74 Cards in this Set

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  • Back
What are the 3 main things that characterize Metabolic Syndrome?
-Insulin resistance
What is the opposite of hunger?
What controls hunger and satiety?
The hypothalamus
What is the immediate acute effect of food intake?
As the stomach distends the vagus nerve sends input to the brain to tell it that its full
What does the presence of food in the stomach/GI tract stimulate?
Release of hormones to stimulate pancreatic secretions including Insulin
What do bloodstream Glu/AA and insulin do after the absorption of nutrients from the GI tract?
Inhibit the hypothalamus
What do absorbed nutrients do to adipose mass?
Stimulates it to release leptin
What does leptin do?
Inhibits the hypothalamus
And what is the effect of the hypothalamus being inhibited by Leptin, Insulin, Glu/AA, and Gastric distention?
Takes away the feeling of hunger so you stop eating
Do patients with diabetes lack leptin?
Why are obese people fat if they still have leptin?
They are leptin resistant.
What 3 GI hormones are released by the intestines in response to food ingestion? What do they do?
They inhibit further feeding
What is Ghrelin? Where is it from? When is it released? What does it do?
Ghrelin is released from the stomach during fasting; it stimulates appetite
Why is Ghrelin special?
Because it is one of the only stimulatory things released from the GI tract - the other hormones and vagus nerve inhibit the hypothalamus
When does Leptin release increase?
When adipose cells get larger
Why does leptin release increase with increase fatness?
To try to make the body lose weight by inhibiting hunger.
Is leptin only made in adipocytes?
No it is made in many other tissues
Leptin correlates with
Fat mass
Function of Leptin:
To act with the hypothalamus to increase satiety and decrease hunger.
What will happen to leptin secretion when:
-Body fat is low
-Body fat is stable
-Body fat is high
Low: leptin release is low until more fat is gained
Stable: stable
High: leptin release is high until fat is lost
Obese: high levels of leptin released at a constant rate
How does obesity develop?
Over many years, the increase in body fat is gradual, so the body fails to notice the increasing leptin levels and is resistant to leptin's effects.
So what are 3 syndromes of endocrine resistance that we know of? What is the hormone and proper name of each?
Vasopressin resistance (Nephrogenic Diabetes Insipidus)
Insulin resistance (Type II DM)
Leptin resistance (Obesity)
Where leptin acts to induce satiety, Ghrelin acts to:
Increase hunger
What can reduce ghrelin?
Bariatric surgeries
What would decrease the desire to snack between meals?
A ghrelin antagonist.. then we wouldn't eat all our little cheese snacks in class.
What are the 3 things that control Hunger in the Short term?
1. Gastric filling/Vagal afferents
2. Increased CCK
3. Decreased Ghrelin
What are the 3 things that control Hunger/Satiety in the Long term?
1. Increase in fat deposition
2. Increased leptin
3. Alterations in NPY/POMC neurons in the hypothalamus
What are the 2 important nuclei in the hypothalamus that control hunger and satiety?
1. Arcuate nucleus
2. Paraventricular nucleus
What 2 types of neurons are in the arcuate nucleus?
1. POMC/CART neurons
2. AGRP/NPY neurons
What do POMC neurons release?
a-MSH and CART
What is the primary action of a-MSH and CART?
Turn off food intake and increase energy expenditure
What do AGRP/NPY neurons release?
What are the primary actions of AGRP and NPY?
Turn ON food intake and DECREASE energy expenditure
Where does a-MSH released by POMC neurons go?
To MCR-3 and MCR-4 - its receptors in the PVN
What happens when a-MSH binds its receptors in the PVN?
It activates neuronal pathways that project to the NTS and increase SNS activity and energy expenditure.
What does AGRP do?
Acts as an antagonist of MCR-4, the a-MSH receptor in the PVN
Result of AGRP antagonizing MCR-4 receptors:
Increased food intake and DECREASED energy expenditure
What do Insulin, CCK, and Leptin act on? What is the result?
-STIMULATE POMC/CART neurons to decrease food intake
What hormone ACTIVATES AGRP/NPY neurons? result?
Ghrelin - stimulates food intake
What would an MC4 agonist do?
Stimulate the a-MSH receptor in the PVN and inhibit food intake
What would happen if you invented an MC4 agonist?
You'd be rich and could live for ever in Tahiti bc you'd have cured obesity
So the peripheral hormones that control hypothalamic hunger and satiety centers are:
The 2 things controlled by the PVN are:
-Energy expenditure
What is going on in an obese person?
Their abnormally high leptin levels are failing to decrease hunger appropriately, and they are failing to increase energy expenditure.
So what are the 2 problems in obese people due to leptin resistance?
-Failure to stop eating
-Decreased basal metabolic rate
What is the cure for Type II Diabetes and Obesity?
Diet and exercise
What is obesity?
A nationwide epidemic that is becoming worse in underdeveloped countries too
What happened between 1971 and 1976?
-Mcdonalds opened
-Cars and TVs proliferated
-Child obesity skyrocketed
How do we cure obesity now?
By stomach stapling - bariatric surgery
How do you do Bariatric surgery?
By detaching the jejunum from the duodenum and reattaching it to the top of the stomach.
Why do you need to retain a little stomach during bariatric surgery?
To still get intrinsic factor which is made in the stomach.
How does stomach stapling help with weight loss?
Because the stomach is so small, it's almost always full, so Ghrelin is always low.
How does the WHO define Metabolic Syndrome?
-Insulin resistance + 2:
How is insulin resistance diagnosed?
By measuring fasting blood sugar, which is elevated but not high enough to meet the diagnostic criteria for DMII
What is visceral obesity?
Belly fat
Why is microalbuminuria bad?
Because normally the glomerulus filters NO protein; small amounts of albumin indicate a decrease in renal function.
What are 2 broad categories of causes of metabolic syndrome?
1. Environmental factors
2. Genetic factors
What is the Thrifty gene?
The gene that makes the body hold onto calories in case it's your last meal.
What are 3 Environmental factors that contribute to metabolic syndrome?
1. Sedentary lifestyle
2. Food intake/type
3. Early life programming
What are examples of early life programming?
-Birth weight
-Stress in the postnatal period
-Stress after the postnatal period
What is the definition of Insulin Resistance?
An inability to increase glucose uptake by cells for the same amount of insulin.
What results from Insulin resistance?
Why is it so bad when people are obese?
Because instead of staying where it belongs in adipocytes, the fat becomes deposited in spaces within the liver, muscles, and beta cells of the islets.
What happens when fat gets deposited in the islets?
It decreases their output of insulin
What is Lipodystrophy?
Low birth weight
What is the adverse effect of lipodystrophy?
There is a reduced capacity to store fat, so it gets deposited in ectopic places as in obesity.
How can you tell apart obesity vs lipodystrophy?
Lipodystrophy has a below normal total amount of fat; obesity obviously has above normal.
What are babies with lipodystrophy programmed to get?
Metabolic syndrome
What distinguishes adults with diabetes due to lipodystrophy from obese diabetics?
They are lean
What is lipotoxicity?
The ectopic fat deposition in the liver, muscle, and islet beta cells
Why do we say that patients with metabolic syndrome have a "Relative Insulinopenia"?
Because they actually have increased insulin levels, but they are below the level needed to function adequetely.
What are 4 major longterm repercussions of metabolic syndrome?
1. Glucose intolerance
2. Dyslipidemia
3. Hypertension
4. Thrombosis
What is the major adverse effect that results from the 4 chronic repercussions?
Vascular/Heart disease
What is the only way to deal with metabolic syndrome?
Behavioral changes