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Permanent Weight Reduction after Abdominoplasty:
Neurocrine Factors,
A Pilot Study

Rex Moulton-Barrett, MD & Jennifer Fuller, B.A.
Plastic & Reconstructive Surgery
Alameda and Brentwood, Ca
The Role for Abdominoplasty ?

Just because you can, does not mean you should ?
After Abdominoplasty
Some Patients:
Lost weight
&
Lost no weight
•
Questions
• Does abdominoplasty lead to long-term weight loss ?
• Which group of patient’s benefit most ?
• What are the cause(s) of weight loss after surgery ?
Obesity Epidemic
• BMI: Body Mass Index: weight kg/(height m) 2
• <1/3 of U.S.
19-25

Normal

• 1/3 of U.S.
25-30

Overweight

• 1/3 of U.S.
BMI 30-40

BMI

Obese

BMI

• The prevalence of obesity has more than doubled since
1980
• 3% of U.S.
BMI> 40

Morbid-Super Obese
Treatment of Obesity
3 main methods of treatment:
•

Life Style Modification
– Moderately effective but difficult to monitor and sustain

•

Pharmacological Therapy
– Few effective treatments exist

•

Surgical Treatment
– Significant and permanent weight loss
– Insurance criteria morbid obesity (BMI ≥40)
Life Style Modification
• Convert to ‘ negative energy gap ’
• Increased energy expenditure:
reduce non-active time: car, chair, sofa
increased exercise time
increased energy lost during exercise
• Diet: high protein
low carbohydrate
low sugar
‘+ ketogenic diets’ reduce appetite
( Am J of Clin Nutrition, 2008: 87(1), 44-55 )

avoid exercise before meals: 20 minute run =

20oz
ie avoid post exercise ‘calorie rewards’
Current Weight Reduction Drugs

( 1% of 59 billion dollars spent to loose fat in USA / yr )

1997:fen-phen (fenfluramine-phentermine) &
Redux (dexfenfluramine) removed from market
% body weight lost

% pts lost at least

minus placebo

5% body weight
a.c.t. placebo ‘/x’

• FDA Approved
– Meridia: Sibutramine
– Xenical: Orllstat

4.3
2.9

55/27
54/33

9.0
4.6
3.4

67/19
53/21
47/23

• New drugs pending approval
– Qnexa
– Contrave
– Lorcaserin
Mechanism of Action
• Meredia: Monoamine RI (serotonin & noradrenaline)
(Abbott) may
BP, HR: not to use if hypertensive
unlike fenfluramine does not elevate serum serotonin
controls binge eating
• Qnexa:
(Vivus)

Phentermine & Topiramate
56 week course: 37 lb loss: BP, glucose, cholesterol
may be useful in type 2 DM
Phentermine: hypothalamic norepinephrine release
high dose: potential for dependence
Topiramate: ( Topamax ), anti-epileptic,
anti-migraine,
bipolar/binge eating
Surgical Treatment
Gastric Bands
Partial Gastric & Intestinal Bypass
( Roux en Y )

Abdominoplasty ?
Abdominoplasty Work-Up
• Obese versus abdominal laxity or symptomatic pannus ?
• First consultation: attempt weight reduction if >200lbs
• Charge about 25% more if over 200lbs
• ‘3 S plan’: South Beach Diet, Sugarless house, Stationary
bike with 45 minute 3x week TV contract after meals
• + Meridia if unsuccessful > 4 weeks & binge eating ?
Abdominoplasty Technique
•
•
•
•

•
•
•
•
•

Low incision 4 cm above the anterior labial commissure
Aggressive midline Rectus Abdominus plication
Jack knife sitting / Trendelenburg position closure
Closure: interrupted Scarpa’s fascia
running dermal barbed 3.0 V -Lock Suture
skin glue and 1 inch Steri-Strips
Lateral flank liposuction for contour
5 day pain pump & overnight in surgery center
Rented surgical bed at home for 2-4 weeks
Prolonged paper taping for 6 months when clothed
3 S’s starting 6 weeks post-op
Methods
•

Retrospective case review: chart & structured
interview

•

same surgeon and one post-graduate student

•

n= 21 patients post-abdominoplasty

• Follow up to > 1 year: 2007-2009
Methods
Data collected included:
• Age, sex, and height

• Previous bariatric surgery ?

• Weight prior to abdominoplasty

• Changes in satiety

• Minimum weight and time attained

• Patient’s beliefs about cause of wt
loss

• Time when weight regained
• Weight at 1 year post-surgery
• Current Weight
• Complications of surgery

• Patient satisfaction with surgical
results
• Changes in diet & exercise after
surgery
• Weight of pannus resected
Results: Patient Population
 5/21 patients previously underwent bariatric
surgery
Range

Mean

Age

21-61 years

45 years

Height

5’0” – 6’0”

5’5”

Pre-op Weight

105-245 lbs

167.5 lbs

Pannus Weight

1.8 – 12.5 lbs

5.74 lbs
Results: BMI’s
My patients BMI mean: 27.66, lowest 18, highest 33.5
My patients
BMI
US population
• 21 %
Normal
33 %
• 50 %
Overweight
33 %
• 29 %
Obese
33 %
• None
Morbid Obesity
3%
Results: Patient Weight loss

• 90.5 % reported weight loss
• 47.6% maintained weight loss > 1 yr after surgery
Results: Patient Weight Loss
Percent of Mean
Patients
Pre-op
Weight
(lbs)

Mean
Maximum
Weight
loss (lbs)

Mean Time
of Max
Weight Loss
(months)

Mean Time of
Weight Regain
(months)

Short term
weight loss
only (<1 year)
n=9

42.9

161.8

8.7

2.3

7.1

Long term
weight loss
(> 1 year)
n=10

47.6

170.4

16.4

3.7

___

9.5

175.5

___

___

___

No Weight loss
n=2
Results: Patient Weight loss
Weight loss as a function of Pannus Weight:

Weight of
Pannus

No. of
Patients

Pre-op
Weight

Maximum
weight loss

% with long-term
weight loss
(> 1 year)

≤ 4 lbs

7

144.9

5.3

33 %

> 4 lbs

14

178.7

14.7

54 %
Results: Patient Weight Loss
• The greatest predictor of weight loss: pre-operative weight
Pre-op Weight
(lbs)

No. of
Patients

Mean
Weight of
Pannus
(lbs)

Mean
Maximum
Weight
Loss (lbs)

Mean Time
Max Weight
Loss reached
(months)

No. Patients
with long
term weight
loss (>1year)

< 140 lbs

4

2.5

1.8

1.4

0

140 ≥ to < 210

14

5.6

15

3.5

9 (64.3%)

≥ 210

3

9.2

8.6

2.2

1 (33.3%)
Pre-operative weight associated with
long term weight loss
WEIGHT
(LBS)

LONG TERM
WEIGHT LOSS
( >/= 4lbs & >1 YR )

< 140 & ≥ 210

1

6

≥ 140 to 210

9

5

p<0.0005

NO LONG TERM
WEIGHT LOSS
( < 4lbs & > 1 YR )
Pre-operative BMI associated With
long term weight loss
BMI

LONG TERM
WEIGHT LOSS
( >/= 4lbs & >1 YR )

<24.5 & ≥ 33.5

1

8

≥ 24.5 to <33.5

9

3

p<0.0023

NO LONG TERM
WEIGHT LOSS
( < 4lbs & > 1 YR )
Results: Weight Loss & Satiety
No
change
in
appetite
(%)

Sense of satiety
only after
eating (%)

Lack of
appetite at
all times (%)

Unpleasant
abdominal
sensation

2 (22.2)

4 (44.4)

3 (33.3)

2 (22.2)

Long-term
weight loss
(>1 year)
n=10

1 (10)

4 (40)

5 (50)

1 (10)

No weight
loss
n=2

2 (100)

0 (0)

0 (0)

0 (0)

All Patients
n=21

5 (23.8)

8 (38.1)

8 (38.1)

3 (14.3)

Short-term
weight loss
only (<1year)
n=9
Reason(s) for Weight Loss

•

Most frequent reason sited for weight loss: increased sense of satiety

•

84.2 % experienced an increase in satiety
– 1/2 report satiety throughout the day, 1/2 report satiety only after eating

•

90% of long-term weight loss patients: reported increased satiety

•

Mean duration of sense of satiety 7.3 months
Conclusions
• The greatest predictor of long-term weight
loss was pre-operative weight then BMI
• 64.3% of patients weighing between 140
and 210 lbs had long term weight loss
• Only 14.3 % of patients outside this range
had long-term weight loss
Conclusions
• The key factor in patient weight loss is
an increase in satiety

• Short-term weight loss patients began
to regain their weight at 7.1 months,
about the same time when their
satiety dissipated
CNS Regulation of
Appetite / Satiety

2 Areas :
The Hypothalamus
• One of the Hypothalamic Nuclei is called
the Arcuate Nucleus (ARC)
• ARC incomplete blood-brain barrier
• Allows CNS entry of peripheral peptides
and proteins
The ARC
• ARC contains two major populations of
neurotransmitter releasng neurons :

• stimulate feeding:
– agouti-related peptide (AgRP) & neuropeptide Y (NPY)

• inhibit feeding:
– Cocaine & amphetamine regulated transcript (CART) &
proopiomelanocortin (POMC),
– POMC cleaves into α -MSH.

Neural/ endocrine
signals

↑ Feeding
2 nd order
neurons

ARC
Hypothalamus

α-MSH

↓ Feeding
The ARC
∀ α -MSH acts as a ligand at the melanocortin - 4
receptor ( MC4 )
• Defects of this receptor: implicated in up to 46% of all
monogenetic childhood onset obesity in
humans
∀ α -MSH inhibits the receptor to AgRP: inhibiting
appeptite
• AgRP inhibits the MC4 receptor: stimulating
appetite
The Brainstem
Appetite signals:
A. from circulating hormones via the area
postrema: incomplete blood-brain
barrier
B. neural signals from the vagus nerve
C. Bidirectional connections with
hypothalamus
The Vagus Nerve

• Afferent signals: mechanical & chemical
• Cell bodies of afferent neurons in the Nodose Ganglia

• Projects into brainstem to interface with hypothalamus
The Vagus Nerve Continued
• The stretch receptor stimulation
dependent on gastric volume
• May suppress meal size independent of content
• Effect is abolished by subdiaphragmatic vagotomy
• Gastric distension is insufficient to account for all
aspects of satiety
The Vagus Nerve
• Contains receptors for a number of gut
hormones
• Vagotomy abolishes appetite-modifying
action of
many gut hormones: CCK, PYY, GLP-1
• Vagus nerve is thought to be a major
sight of gut hormone signaling
A Very Quick Overview of Appetite
Regulating Hormones
Appetite-regulating hormones:
• Ghrelin, released from the stomach, is the only known appetite
stimulant, acting via hypothalamic expression of NPY and AgRP.
– Ghrelin levels rise preprandially in humans
– Administration of exogenous ghrelin leads to increased food intake and
weight gain
Appetite-regulating Hormones:
• In contrast, a growing number of peptide hormones have been found to
produce satiety and decrease food intake.

Vagus
Nerve

Pancreatic
Polypeptide (PP)
Amylin
Insulin

Peptide YY (PYY)
Cholecystokinin (CCK)

Adiponectin
Leptin

Oxyntomodulin (OXM)
Apolipoprotein A-IV (apo A-IV)
Vasoactive Intestinal
Polypeptide (VIP)
Glucagon-like peptide-1
(GLP-1)

Bombesin
Energy
Regulation

Summary: Gut Hormones
PP

Pancreas

-

+
Vagu
s

Ghrelin

Stomac
h

-

PP
Bombesi
n

CC
K
PYY
GLP1
OX
M
VIP
Apo A-IV

Intestines
Another Important Satiety
Regulator: Leptin
• Leptin, is released from adipose tissue,
mammary glands, ovarian follicles, placenta,
skeletal muscle, and the P cell and chief cells of
the stomach
• 25% of circulating leptin is derived from the
stomach
• Leptin levels positively correlate with body fat:
higher circulating leptins with greater BMI
• Leptin mediates central regulation of energy
homeostasis via receptors in the ARC and
peripherally via the vagus nerve
Leptin Studies
• after binding in the hypothalamus receptor:
• leptin inhibits NPY and AgRP and
stimulates POMC and CART
• decreasing appetite & increasing energy expenditure
(Cowley M, et al; Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus. 2001)

• mice with mutation of the Leptin receptor are profoundly obese.
(Farooqi I, et al; Clinical and molecular genetic spectrum of congenital deficiency of the leptin receptor. 2007)

Ob /Ob mouse
Appetite-regulating hormones:
• Starvation:

: ghrelin,

: PYY-3-36, insulin, leptin

• Post-prandial satiety:

: ghrelin,

: PYY-3-36, insulin, leptin

• Receptor mutations: CCK, OXM, insulin, PYY, leptin & bombesin
: food intake and obesity
• Receptor antagonist or antisera for CCK, OXM, apo A-IV, PYY, and GLP-1
: food intake
• Jejuno-ileal bypass surgery or vertical-banded gastroplasty
: GLP-1, PYY & PP levels
• Roux-en-Y :

: 77% reduction in serum ghrelin

• 2 clinical studies from U London:
a. s/cut injections CCK: Med students ate 25% less curry
b. s/cut Modulin: 17 % less food intake & 26 % increased energy expenditure
: 1 pound / wk. weight loss
Future Study
• Patients are tested before abdominoplasty and
incrementally after for levels of specific gut hormones
• Is there an association between hormone expression
levels, reported satiety, and patient weight loss?
Methods

• 15 patients to participate in our study
• Prior to surgery: age, weight, height, gynecological history, previous
bariatric surgeries, and exercise regimens
• Fasting blood draw: Prior to & 1, 3, 6, and 12 months after surgery
• At surgery weight of the pannus will be recorded
Methods
• Blood plasma specimens will be shipped to Inter Science Institute on
dry ice then assayed for PYY, GLP-1, PP, CCK, leptin, bombesin, and
ghrelin
• At 0, 1, 3, 6, and 12 months post-abdominoplasty, document:
– Ranking on a 0-3 scale of:
» Appetite at rest
» Postprandial satiety
» Unpleasant abdominal feeling associated with poor appetite
» Amount of food consumed during a meal
Budget
Long Term Weight Loss Following Abdominoplasty: Neurocrine Factors

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Long Term Weight Loss Following Abdominoplasty: Neurocrine Factors

  • 1. Permanent Weight Reduction after Abdominoplasty: Neurocrine Factors, A Pilot Study Rex Moulton-Barrett, MD & Jennifer Fuller, B.A. Plastic & Reconstructive Surgery Alameda and Brentwood, Ca
  • 2. The Role for Abdominoplasty ? Just because you can, does not mean you should ?
  • 3. After Abdominoplasty Some Patients: Lost weight & Lost no weight •
  • 4. Questions • Does abdominoplasty lead to long-term weight loss ? • Which group of patient’s benefit most ? • What are the cause(s) of weight loss after surgery ?
  • 5. Obesity Epidemic • BMI: Body Mass Index: weight kg/(height m) 2 • <1/3 of U.S. 19-25 Normal • 1/3 of U.S. 25-30 Overweight • 1/3 of U.S. BMI 30-40 BMI Obese BMI • The prevalence of obesity has more than doubled since 1980 • 3% of U.S. BMI> 40 Morbid-Super Obese
  • 6. Treatment of Obesity 3 main methods of treatment: • Life Style Modification – Moderately effective but difficult to monitor and sustain • Pharmacological Therapy – Few effective treatments exist • Surgical Treatment – Significant and permanent weight loss – Insurance criteria morbid obesity (BMI ≥40)
  • 7. Life Style Modification • Convert to ‘ negative energy gap ’ • Increased energy expenditure: reduce non-active time: car, chair, sofa increased exercise time increased energy lost during exercise • Diet: high protein low carbohydrate low sugar ‘+ ketogenic diets’ reduce appetite ( Am J of Clin Nutrition, 2008: 87(1), 44-55 ) avoid exercise before meals: 20 minute run = 20oz ie avoid post exercise ‘calorie rewards’
  • 8. Current Weight Reduction Drugs ( 1% of 59 billion dollars spent to loose fat in USA / yr ) 1997:fen-phen (fenfluramine-phentermine) & Redux (dexfenfluramine) removed from market % body weight lost % pts lost at least minus placebo 5% body weight a.c.t. placebo ‘/x’ • FDA Approved – Meridia: Sibutramine – Xenical: Orllstat 4.3 2.9 55/27 54/33 9.0 4.6 3.4 67/19 53/21 47/23 • New drugs pending approval – Qnexa – Contrave – Lorcaserin
  • 9. Mechanism of Action • Meredia: Monoamine RI (serotonin & noradrenaline) (Abbott) may BP, HR: not to use if hypertensive unlike fenfluramine does not elevate serum serotonin controls binge eating • Qnexa: (Vivus) Phentermine & Topiramate 56 week course: 37 lb loss: BP, glucose, cholesterol may be useful in type 2 DM Phentermine: hypothalamic norepinephrine release high dose: potential for dependence Topiramate: ( Topamax ), anti-epileptic, anti-migraine, bipolar/binge eating
  • 10. Surgical Treatment Gastric Bands Partial Gastric & Intestinal Bypass ( Roux en Y ) Abdominoplasty ?
  • 11. Abdominoplasty Work-Up • Obese versus abdominal laxity or symptomatic pannus ? • First consultation: attempt weight reduction if >200lbs • Charge about 25% more if over 200lbs • ‘3 S plan’: South Beach Diet, Sugarless house, Stationary bike with 45 minute 3x week TV contract after meals • + Meridia if unsuccessful > 4 weeks & binge eating ?
  • 12. Abdominoplasty Technique • • • • • • • • • Low incision 4 cm above the anterior labial commissure Aggressive midline Rectus Abdominus plication Jack knife sitting / Trendelenburg position closure Closure: interrupted Scarpa’s fascia running dermal barbed 3.0 V -Lock Suture skin glue and 1 inch Steri-Strips Lateral flank liposuction for contour 5 day pain pump & overnight in surgery center Rented surgical bed at home for 2-4 weeks Prolonged paper taping for 6 months when clothed 3 S’s starting 6 weeks post-op
  • 13.
  • 14. Methods • Retrospective case review: chart & structured interview • same surgeon and one post-graduate student • n= 21 patients post-abdominoplasty • Follow up to > 1 year: 2007-2009
  • 15. Methods Data collected included: • Age, sex, and height • Previous bariatric surgery ? • Weight prior to abdominoplasty • Changes in satiety • Minimum weight and time attained • Patient’s beliefs about cause of wt loss • Time when weight regained • Weight at 1 year post-surgery • Current Weight • Complications of surgery • Patient satisfaction with surgical results • Changes in diet & exercise after surgery • Weight of pannus resected
  • 16. Results: Patient Population  5/21 patients previously underwent bariatric surgery Range Mean Age 21-61 years 45 years Height 5’0” – 6’0” 5’5” Pre-op Weight 105-245 lbs 167.5 lbs Pannus Weight 1.8 – 12.5 lbs 5.74 lbs
  • 17. Results: BMI’s My patients BMI mean: 27.66, lowest 18, highest 33.5 My patients BMI US population • 21 % Normal 33 % • 50 % Overweight 33 % • 29 % Obese 33 % • None Morbid Obesity 3%
  • 18. Results: Patient Weight loss • 90.5 % reported weight loss • 47.6% maintained weight loss > 1 yr after surgery
  • 19. Results: Patient Weight Loss Percent of Mean Patients Pre-op Weight (lbs) Mean Maximum Weight loss (lbs) Mean Time of Max Weight Loss (months) Mean Time of Weight Regain (months) Short term weight loss only (<1 year) n=9 42.9 161.8 8.7 2.3 7.1 Long term weight loss (> 1 year) n=10 47.6 170.4 16.4 3.7 ___ 9.5 175.5 ___ ___ ___ No Weight loss n=2
  • 20. Results: Patient Weight loss Weight loss as a function of Pannus Weight: Weight of Pannus No. of Patients Pre-op Weight Maximum weight loss % with long-term weight loss (> 1 year) ≤ 4 lbs 7 144.9 5.3 33 % > 4 lbs 14 178.7 14.7 54 %
  • 21. Results: Patient Weight Loss • The greatest predictor of weight loss: pre-operative weight Pre-op Weight (lbs) No. of Patients Mean Weight of Pannus (lbs) Mean Maximum Weight Loss (lbs) Mean Time Max Weight Loss reached (months) No. Patients with long term weight loss (>1year) < 140 lbs 4 2.5 1.8 1.4 0 140 ≥ to < 210 14 5.6 15 3.5 9 (64.3%) ≥ 210 3 9.2 8.6 2.2 1 (33.3%)
  • 22. Pre-operative weight associated with long term weight loss WEIGHT (LBS) LONG TERM WEIGHT LOSS ( >/= 4lbs & >1 YR ) < 140 & ≥ 210 1 6 ≥ 140 to 210 9 5 p<0.0005 NO LONG TERM WEIGHT LOSS ( < 4lbs & > 1 YR )
  • 23. Pre-operative BMI associated With long term weight loss BMI LONG TERM WEIGHT LOSS ( >/= 4lbs & >1 YR ) <24.5 & ≥ 33.5 1 8 ≥ 24.5 to <33.5 9 3 p<0.0023 NO LONG TERM WEIGHT LOSS ( < 4lbs & > 1 YR )
  • 24. Results: Weight Loss & Satiety No change in appetite (%) Sense of satiety only after eating (%) Lack of appetite at all times (%) Unpleasant abdominal sensation 2 (22.2) 4 (44.4) 3 (33.3) 2 (22.2) Long-term weight loss (>1 year) n=10 1 (10) 4 (40) 5 (50) 1 (10) No weight loss n=2 2 (100) 0 (0) 0 (0) 0 (0) All Patients n=21 5 (23.8) 8 (38.1) 8 (38.1) 3 (14.3) Short-term weight loss only (<1year) n=9
  • 25. Reason(s) for Weight Loss • Most frequent reason sited for weight loss: increased sense of satiety • 84.2 % experienced an increase in satiety – 1/2 report satiety throughout the day, 1/2 report satiety only after eating • 90% of long-term weight loss patients: reported increased satiety • Mean duration of sense of satiety 7.3 months
  • 26. Conclusions • The greatest predictor of long-term weight loss was pre-operative weight then BMI • 64.3% of patients weighing between 140 and 210 lbs had long term weight loss • Only 14.3 % of patients outside this range had long-term weight loss
  • 27. Conclusions • The key factor in patient weight loss is an increase in satiety • Short-term weight loss patients began to regain their weight at 7.1 months, about the same time when their satiety dissipated
  • 28. CNS Regulation of Appetite / Satiety 2 Areas :
  • 29. The Hypothalamus • One of the Hypothalamic Nuclei is called the Arcuate Nucleus (ARC) • ARC incomplete blood-brain barrier • Allows CNS entry of peripheral peptides and proteins
  • 30. The ARC • ARC contains two major populations of neurotransmitter releasng neurons : • stimulate feeding: – agouti-related peptide (AgRP) & neuropeptide Y (NPY) • inhibit feeding: – Cocaine & amphetamine regulated transcript (CART) & proopiomelanocortin (POMC), – POMC cleaves into α -MSH. Neural/ endocrine signals ↑ Feeding 2 nd order neurons ARC Hypothalamus α-MSH ↓ Feeding
  • 31. The ARC ∀ α -MSH acts as a ligand at the melanocortin - 4 receptor ( MC4 ) • Defects of this receptor: implicated in up to 46% of all monogenetic childhood onset obesity in humans ∀ α -MSH inhibits the receptor to AgRP: inhibiting appeptite • AgRP inhibits the MC4 receptor: stimulating appetite
  • 32. The Brainstem Appetite signals: A. from circulating hormones via the area postrema: incomplete blood-brain barrier B. neural signals from the vagus nerve C. Bidirectional connections with hypothalamus
  • 33. The Vagus Nerve • Afferent signals: mechanical & chemical • Cell bodies of afferent neurons in the Nodose Ganglia • Projects into brainstem to interface with hypothalamus
  • 34. The Vagus Nerve Continued • The stretch receptor stimulation dependent on gastric volume • May suppress meal size independent of content • Effect is abolished by subdiaphragmatic vagotomy • Gastric distension is insufficient to account for all aspects of satiety
  • 35. The Vagus Nerve • Contains receptors for a number of gut hormones • Vagotomy abolishes appetite-modifying action of many gut hormones: CCK, PYY, GLP-1 • Vagus nerve is thought to be a major sight of gut hormone signaling
  • 36. A Very Quick Overview of Appetite Regulating Hormones
  • 37. Appetite-regulating hormones: • Ghrelin, released from the stomach, is the only known appetite stimulant, acting via hypothalamic expression of NPY and AgRP. – Ghrelin levels rise preprandially in humans – Administration of exogenous ghrelin leads to increased food intake and weight gain
  • 38. Appetite-regulating Hormones: • In contrast, a growing number of peptide hormones have been found to produce satiety and decrease food intake. Vagus Nerve Pancreatic Polypeptide (PP) Amylin Insulin Peptide YY (PYY) Cholecystokinin (CCK) Adiponectin Leptin Oxyntomodulin (OXM) Apolipoprotein A-IV (apo A-IV) Vasoactive Intestinal Polypeptide (VIP) Glucagon-like peptide-1 (GLP-1) Bombesin
  • 40. Another Important Satiety Regulator: Leptin • Leptin, is released from adipose tissue, mammary glands, ovarian follicles, placenta, skeletal muscle, and the P cell and chief cells of the stomach • 25% of circulating leptin is derived from the stomach • Leptin levels positively correlate with body fat: higher circulating leptins with greater BMI • Leptin mediates central regulation of energy homeostasis via receptors in the ARC and peripherally via the vagus nerve
  • 41. Leptin Studies • after binding in the hypothalamus receptor: • leptin inhibits NPY and AgRP and stimulates POMC and CART • decreasing appetite & increasing energy expenditure (Cowley M, et al; Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus. 2001) • mice with mutation of the Leptin receptor are profoundly obese. (Farooqi I, et al; Clinical and molecular genetic spectrum of congenital deficiency of the leptin receptor. 2007) Ob /Ob mouse
  • 42. Appetite-regulating hormones: • Starvation: : ghrelin, : PYY-3-36, insulin, leptin • Post-prandial satiety: : ghrelin, : PYY-3-36, insulin, leptin • Receptor mutations: CCK, OXM, insulin, PYY, leptin & bombesin : food intake and obesity • Receptor antagonist or antisera for CCK, OXM, apo A-IV, PYY, and GLP-1 : food intake • Jejuno-ileal bypass surgery or vertical-banded gastroplasty : GLP-1, PYY & PP levels • Roux-en-Y : : 77% reduction in serum ghrelin • 2 clinical studies from U London: a. s/cut injections CCK: Med students ate 25% less curry b. s/cut Modulin: 17 % less food intake & 26 % increased energy expenditure : 1 pound / wk. weight loss
  • 43. Future Study • Patients are tested before abdominoplasty and incrementally after for levels of specific gut hormones • Is there an association between hormone expression levels, reported satiety, and patient weight loss?
  • 44. Methods • 15 patients to participate in our study • Prior to surgery: age, weight, height, gynecological history, previous bariatric surgeries, and exercise regimens • Fasting blood draw: Prior to & 1, 3, 6, and 12 months after surgery • At surgery weight of the pannus will be recorded
  • 45. Methods • Blood plasma specimens will be shipped to Inter Science Institute on dry ice then assayed for PYY, GLP-1, PP, CCK, leptin, bombesin, and ghrelin • At 0, 1, 3, 6, and 12 months post-abdominoplasty, document: – Ranking on a 0-3 scale of: » Appetite at rest » Postprandial satiety » Unpleasant abdominal feeling associated with poor appetite » Amount of food consumed during a meal