LATEST 2024 OBESITY MEDICINE BOARD EXAM (ABOM)
EXAM / OBESITY MEDICINE BOARD REAL EXAM
TESTBANK ALL 500 ACTUAL EXAM QUESTIONS AND
WELL ELABORATED ANSWERS (VERIFIED ANSWERS) A
NEW UPDATED VERSION 2024 | GUARANTEED PASS A+
(BRAND NEW!!)
Ghrelin - ANSWER: -only known orexigenic gut hormone
-inactive form --ghrelin O-acyltransferase (GOAT)--ghrelin-acyl (active form)
-Growth Hormone Release Inducing Peptide
-secreted by: gastric fundus/body, proximal small intestine (decreased w/ sleeve
gastrectomy--remove greater curvature of stomach/fundus)
+: empty stomach, weight loss, stress, sleep deprivation, genetics (Prader willi)
-: stomach stretch*^, weight gain, leptin, gastric sleeve--*occurs less in pts w/
obesity, ^inhibited fastest by CHO, but also rebounds fastes, protein - the longest
-fx: + NPY/AgRP in CNS (arcuate nucleus in hypthalamus) +/- activation of nucleus
tractus solitarius through vagal nerve (vagotomy - ghrelin); + gut motility, - insulin
secretion
Ghrelin and weight loss - ANSWER: -ghrelin levels increase as you lose weight
-weight regain-->reduced ghrelin levels
-obesity-->reduced decrease in ghrelin post-prandial meals
Small Intestine Hormones - ANSWER: -short acting, reduce appetite
-goal: cause meal termination
-CCK (cholecystokinin)
-GLP-1 (glucagon-like peptide 1_
-OXM (oxytomodulin)
-PYY (peptide YY)
CCK (Cholecystokinin) - ANSWER: -released from sm. intestinal I-cells (duodenum
and jejunum)
+: fat/protein ingestion, gastric distension
-short acting (15-30 min)
-act on rec's in gut and brain:
-CCK-1 rec=GI=slow gastric emptying and + gallbladder contraction
-CCK-2 rec = brain = reduce appetite
-poor pharm studies b/c too short acting and develop tolerance
GLP-1 - ANSWER: -from L-cells of distal sm. int and colon
+ by: nutrient intake (CHO>protein/fat)
-"incretin" effects: 1) glucose dep't insulin secretion (1st phase insulin response)
2)reduced hepatic gluconeogenesis (supresses glucagon) 3) delayed gastric emptying
(increased satiety) 4) reduced appetite (weight loss)
,-1/2 life = 5min (degraded by DPP-4)
GLP-1 and obesity - ANSWER: -GLP-1 levels are reduced in: obesity, pre-DM, T2DM
(by enzyme in proximal sm. intestine)
-gastric bypass skips over this inhibitory part of sm. int-->increased GLP-1 levels (why
T2DM pts resolve DM quickly even before they lose weight)
OXM (oxyntomodulin) - ANSWER: -produced by L-cells of distal small bowel (co-
secreted w/ GLP-1) post-prandially
-works on many rec's-->GLP-1 and glucagon (increases E expenditure)
-fx's: decrease appetite/feeding, increase E expenditure, weight loss
-less GI sx's than GLP-1 (good option for trx)
PYY (Peptide YY) - ANSWER: -produced b L-cells of distal sm bowel, colon, rectum
-elevates w/in 1 hr post-feeding
-works on Y2 rec
-fx: potent appetite suppressant/anorexiant, slows gastric emptying and intestinal
tract time ("ileal brake")
-clinical: IV infusion decreased calorie intake x 30% but lots of GI sx's; bariatric
surgery -->natural increase of PYY
GIP (glucose-dependent insulinotropic polypeptide) - ANSWER: -previously gastric-
inhibitory peptide
~ GLP-1 (incretin)=together make up 70% postprandial insulin response
-releasted from intestinal K-cells in duodenum and upper jejunum in response to oral
glucose load
Large Intestine Hormones - ANSWER: -same as sm intestine EXCEPT CCK
-GLP-1, OXM, PYY
Pancreatic hormones - ANSWER: -exocrine (digestion)
-endocrine (glucose homeostatis and reduced feeding):
1. pancreatic polypeptide
2. insulin
3. amylin
Pancreatic Polypeptide (PP) - ANSWER: -made in F-cells of pancreas in response to
calorie load (~ PYY)
-binds to Y4 rec's:
in gut-->reduced gastric emptying
in hypothalamus--> inhibits NPY mRNA expression-->reduced hunger
-obesity is ass'd with lower PP levels (seen in Prader Willi)
Insulin - ANSWER: -secreted by pancreatic B-cells in response to feeding
-fx's: glucose homeostasis and fat mgmt (increases nutrient storage peripherally but
centrally reduces appetite)
,Insulin's adiposopathy homeostasis fx's - ANSWER: -1 of 2 long-term adiposity
signaling hormone:
-circulating levels are proportionate to level of body fat
-in hypothalamus it inhibits feeding (AgRP/NPY neurons)
-similar effect to leptin CENTRALLY, but less potent
-in obesity, insulin resistance attenuates weight-loss effects centrally
Insulin's glucose homeostatis - ANSWER: Muscle: uptake glucose-->glycogen; uptake
aa's-->protein
Liver: uptake glucose-->glycogen; inhibits fats/protein-->glucose
Adipose: + fat synthesis
Glucagon's glucose homeostasis fx's - ANSWER: -from alpha cells of pancreas
-stimulated by low glucose
-inhibited by high glucose, GLP-1, amylin
Liver: +gluconeogenesis (glycogen-->glucose, aa's-->glucose) to keep steady blood
sugar through meals
Amylin - ANSWER: -co-secreted w/ insulin by pancreatic B-cells in response to meals
-fx's: regulates glucose and bodyweight (1. reduces food intake, 2. slows gastric
emptying 3) suppresses glucagon production/hepatic gluconeogenesis) ~GLP-1 but
with less glucose reduction
-makes insulin more effective for glucose lowering
-pharm: pramlintide=amylin analog to reduce insulin need
Pramlintide - ANSWER: -brand name: Symlin
-amylin analog
-FDA approved for T1DM & T2DM
-administered before meals to reduce insulin req's
-a1c reduction: 0.3-0.6%
-weight loss: 3-4# in 6 mo's (more effective when combined with phentermine--11%
TBW loss)
White adipose tissue - ANSWER: -provides insulation
-helps with mechanical support
-contributes to E balance (stores E if excess (as TG's) in large, unilobular drops or
releases TG's to be broken down by lipases-->glycerols or FFA's in times of low E)
Adipocyte Hormones - ANSWER: -leptin
-adiponectin
Leptin - ANSWER: -uses long-term signaling to control body weight (discovered 1994)
-secreted by white adipose tissue
-fx: metabolic signal of energy sufficiency (not excess)--crosses BBB to hypothalamus
to influence appetite/EE corresponding to E needs
+anorexigenic (weight loss) neurons: POMC
-orexigenic (weight gain) neuron system NPY/AgRP
, -circulating levels directly proportional to body fat mass
Leptin Resistance - ANSWER: -high levels of circulating leptin do not cause
anticipated anorexic weight-loss effects
-theories:
1. high level of overstimulation-->deactivation of signaling (~insulin resistance)
2. impairment of leptin crossing BBB inhibits leptin signaling
Leptin Receptor - ANSWER: -found on many different organs
-activates SNS-->increased BP and thermogenic effect of brown fat (why when we
lose weight we reduce BP)
-secreted in diurnal pattern (~circadian rhythm)
-stimulates hypothalamic TRH neurons
-inhibits stress induced hypercortisolism
-interacts with gonadotropin pulse generations (FSH/LH) on hypothalamic-pituitary-
gonadal axes (low body weight amenorrhea/low testosterone)
-hematopoiesis role as well
Adiponectin - ANSWER: -improves insulin sensitivity an d increases with improved IR
-only made in white adipose tissue (most abundantly secreted adipocyte hormone)
-inversely related to body fat mass
-strong inverse relationship with insulin resistance and inflammatory states
(obesity/IR correlate with low adiponectin levels)
-fx's: improves insulin sensitivity in skeletal muscle, liver, and reduces vascular
inflammation
-
arcuate nucleus - ANSWER: -base of hypothalamus
-permeable barrier for signal reception (from GI/adipocyte hormones, nutritiens-
glucose, FA, aa's)
First order neurons - ANSWER: -found in the arcuate nucleus
-receive peripheral signals
-2 neuron systems in AN: NPY/AgRP (weight gain) or POMC/CART (weight loss)
second order neurons - ANSWER: -deep in hypothalamus
-receive signals from first order neurons in arcuate nucleus and send to other parts
of brain
-2 systems: weight gain: NPY->Y1/Y5
weight loss: POMC-->a-MSH-->MC4R (MC4R is blocked by AgRP)
Neuropeptide Y (NPY) - ANSWER: -causes weight gain
-found in first order neurons of Arc N (norm with AgRP)
-most abundant central neuropeptide and most potent orexigen known
-stimulated by ghrelin
-inhibited by insulin, leptin, PP, PYY, and 5HT
-stimulates hunger by acting on Y1/Y5 rec's of second order neurons-->MCH release
EXAM / OBESITY MEDICINE BOARD REAL EXAM
TESTBANK ALL 500 ACTUAL EXAM QUESTIONS AND
WELL ELABORATED ANSWERS (VERIFIED ANSWERS) A
NEW UPDATED VERSION 2024 | GUARANTEED PASS A+
(BRAND NEW!!)
Ghrelin - ANSWER: -only known orexigenic gut hormone
-inactive form --ghrelin O-acyltransferase (GOAT)--ghrelin-acyl (active form)
-Growth Hormone Release Inducing Peptide
-secreted by: gastric fundus/body, proximal small intestine (decreased w/ sleeve
gastrectomy--remove greater curvature of stomach/fundus)
+: empty stomach, weight loss, stress, sleep deprivation, genetics (Prader willi)
-: stomach stretch*^, weight gain, leptin, gastric sleeve--*occurs less in pts w/
obesity, ^inhibited fastest by CHO, but also rebounds fastes, protein - the longest
-fx: + NPY/AgRP in CNS (arcuate nucleus in hypthalamus) +/- activation of nucleus
tractus solitarius through vagal nerve (vagotomy - ghrelin); + gut motility, - insulin
secretion
Ghrelin and weight loss - ANSWER: -ghrelin levels increase as you lose weight
-weight regain-->reduced ghrelin levels
-obesity-->reduced decrease in ghrelin post-prandial meals
Small Intestine Hormones - ANSWER: -short acting, reduce appetite
-goal: cause meal termination
-CCK (cholecystokinin)
-GLP-1 (glucagon-like peptide 1_
-OXM (oxytomodulin)
-PYY (peptide YY)
CCK (Cholecystokinin) - ANSWER: -released from sm. intestinal I-cells (duodenum
and jejunum)
+: fat/protein ingestion, gastric distension
-short acting (15-30 min)
-act on rec's in gut and brain:
-CCK-1 rec=GI=slow gastric emptying and + gallbladder contraction
-CCK-2 rec = brain = reduce appetite
-poor pharm studies b/c too short acting and develop tolerance
GLP-1 - ANSWER: -from L-cells of distal sm. int and colon
+ by: nutrient intake (CHO>protein/fat)
-"incretin" effects: 1) glucose dep't insulin secretion (1st phase insulin response)
2)reduced hepatic gluconeogenesis (supresses glucagon) 3) delayed gastric emptying
(increased satiety) 4) reduced appetite (weight loss)
,-1/2 life = 5min (degraded by DPP-4)
GLP-1 and obesity - ANSWER: -GLP-1 levels are reduced in: obesity, pre-DM, T2DM
(by enzyme in proximal sm. intestine)
-gastric bypass skips over this inhibitory part of sm. int-->increased GLP-1 levels (why
T2DM pts resolve DM quickly even before they lose weight)
OXM (oxyntomodulin) - ANSWER: -produced by L-cells of distal small bowel (co-
secreted w/ GLP-1) post-prandially
-works on many rec's-->GLP-1 and glucagon (increases E expenditure)
-fx's: decrease appetite/feeding, increase E expenditure, weight loss
-less GI sx's than GLP-1 (good option for trx)
PYY (Peptide YY) - ANSWER: -produced b L-cells of distal sm bowel, colon, rectum
-elevates w/in 1 hr post-feeding
-works on Y2 rec
-fx: potent appetite suppressant/anorexiant, slows gastric emptying and intestinal
tract time ("ileal brake")
-clinical: IV infusion decreased calorie intake x 30% but lots of GI sx's; bariatric
surgery -->natural increase of PYY
GIP (glucose-dependent insulinotropic polypeptide) - ANSWER: -previously gastric-
inhibitory peptide
~ GLP-1 (incretin)=together make up 70% postprandial insulin response
-releasted from intestinal K-cells in duodenum and upper jejunum in response to oral
glucose load
Large Intestine Hormones - ANSWER: -same as sm intestine EXCEPT CCK
-GLP-1, OXM, PYY
Pancreatic hormones - ANSWER: -exocrine (digestion)
-endocrine (glucose homeostatis and reduced feeding):
1. pancreatic polypeptide
2. insulin
3. amylin
Pancreatic Polypeptide (PP) - ANSWER: -made in F-cells of pancreas in response to
calorie load (~ PYY)
-binds to Y4 rec's:
in gut-->reduced gastric emptying
in hypothalamus--> inhibits NPY mRNA expression-->reduced hunger
-obesity is ass'd with lower PP levels (seen in Prader Willi)
Insulin - ANSWER: -secreted by pancreatic B-cells in response to feeding
-fx's: glucose homeostasis and fat mgmt (increases nutrient storage peripherally but
centrally reduces appetite)
,Insulin's adiposopathy homeostasis fx's - ANSWER: -1 of 2 long-term adiposity
signaling hormone:
-circulating levels are proportionate to level of body fat
-in hypothalamus it inhibits feeding (AgRP/NPY neurons)
-similar effect to leptin CENTRALLY, but less potent
-in obesity, insulin resistance attenuates weight-loss effects centrally
Insulin's glucose homeostatis - ANSWER: Muscle: uptake glucose-->glycogen; uptake
aa's-->protein
Liver: uptake glucose-->glycogen; inhibits fats/protein-->glucose
Adipose: + fat synthesis
Glucagon's glucose homeostasis fx's - ANSWER: -from alpha cells of pancreas
-stimulated by low glucose
-inhibited by high glucose, GLP-1, amylin
Liver: +gluconeogenesis (glycogen-->glucose, aa's-->glucose) to keep steady blood
sugar through meals
Amylin - ANSWER: -co-secreted w/ insulin by pancreatic B-cells in response to meals
-fx's: regulates glucose and bodyweight (1. reduces food intake, 2. slows gastric
emptying 3) suppresses glucagon production/hepatic gluconeogenesis) ~GLP-1 but
with less glucose reduction
-makes insulin more effective for glucose lowering
-pharm: pramlintide=amylin analog to reduce insulin need
Pramlintide - ANSWER: -brand name: Symlin
-amylin analog
-FDA approved for T1DM & T2DM
-administered before meals to reduce insulin req's
-a1c reduction: 0.3-0.6%
-weight loss: 3-4# in 6 mo's (more effective when combined with phentermine--11%
TBW loss)
White adipose tissue - ANSWER: -provides insulation
-helps with mechanical support
-contributes to E balance (stores E if excess (as TG's) in large, unilobular drops or
releases TG's to be broken down by lipases-->glycerols or FFA's in times of low E)
Adipocyte Hormones - ANSWER: -leptin
-adiponectin
Leptin - ANSWER: -uses long-term signaling to control body weight (discovered 1994)
-secreted by white adipose tissue
-fx: metabolic signal of energy sufficiency (not excess)--crosses BBB to hypothalamus
to influence appetite/EE corresponding to E needs
+anorexigenic (weight loss) neurons: POMC
-orexigenic (weight gain) neuron system NPY/AgRP
, -circulating levels directly proportional to body fat mass
Leptin Resistance - ANSWER: -high levels of circulating leptin do not cause
anticipated anorexic weight-loss effects
-theories:
1. high level of overstimulation-->deactivation of signaling (~insulin resistance)
2. impairment of leptin crossing BBB inhibits leptin signaling
Leptin Receptor - ANSWER: -found on many different organs
-activates SNS-->increased BP and thermogenic effect of brown fat (why when we
lose weight we reduce BP)
-secreted in diurnal pattern (~circadian rhythm)
-stimulates hypothalamic TRH neurons
-inhibits stress induced hypercortisolism
-interacts with gonadotropin pulse generations (FSH/LH) on hypothalamic-pituitary-
gonadal axes (low body weight amenorrhea/low testosterone)
-hematopoiesis role as well
Adiponectin - ANSWER: -improves insulin sensitivity an d increases with improved IR
-only made in white adipose tissue (most abundantly secreted adipocyte hormone)
-inversely related to body fat mass
-strong inverse relationship with insulin resistance and inflammatory states
(obesity/IR correlate with low adiponectin levels)
-fx's: improves insulin sensitivity in skeletal muscle, liver, and reduces vascular
inflammation
-
arcuate nucleus - ANSWER: -base of hypothalamus
-permeable barrier for signal reception (from GI/adipocyte hormones, nutritiens-
glucose, FA, aa's)
First order neurons - ANSWER: -found in the arcuate nucleus
-receive peripheral signals
-2 neuron systems in AN: NPY/AgRP (weight gain) or POMC/CART (weight loss)
second order neurons - ANSWER: -deep in hypothalamus
-receive signals from first order neurons in arcuate nucleus and send to other parts
of brain
-2 systems: weight gain: NPY->Y1/Y5
weight loss: POMC-->a-MSH-->MC4R (MC4R is blocked by AgRP)
Neuropeptide Y (NPY) - ANSWER: -causes weight gain
-found in first order neurons of Arc N (norm with AgRP)
-most abundant central neuropeptide and most potent orexigen known
-stimulated by ghrelin
-inhibited by insulin, leptin, PP, PYY, and 5HT
-stimulates hunger by acting on Y1/Y5 rec's of second order neurons-->MCH release
