Women @ Heart The link between visceral fat and Athersclerosis

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Women _at_ HeartThe link between visceral fat and
Athersclerosis

• By
• Ashraf Reda MD
• Prof and Head of Cardiology Dep
• Menofia university

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If they have menopause men may have andropause
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• Describe the pathophysiology of intra-abdominal
  adiposity.
• Define the role of intra-abdominal adiposity as a
  major cause of cardiometabolic disease.
• Discuss current research related to CB1 blockade
  as a novel approach to cardiometabolic disease
  management.

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(No Transcript)
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Intra-abdominal adipose tissue
Lipolysis
Abdominal obesity
PV
FFAs
Cluster of metabolic CV RFs
Liver
Metabolic syndrome
Hepatic ins.R. Small LDL particles HDL
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VLDL
FFAc
Liver (Fatty liver)
Glucose
B-cells
Insulin
Sk. Msc ( Ectopic fat)
Hyperinulinemia
(Insulin Resistence)
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Effect of plasma FFA
FFA TG
Adipose tissue
Liver
FFA
HL
TG
HDL3
HDL2
CETP
CE
HL
CE
VLDL
CETP
LDL
TG
LDL
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Dyslipidemia not hyperlipidemia

• We have to think both quantitavely and
  qualitatively
• Looking at total cholesterol or LDL level is not
  enough

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Lipid profile among patients with ACS
incardiology dep. Menofia university
No Mean (mg/dl)
TC lt 200mg/dl 25/40 62.5
160.3
Mean BNP 943.2 (N up to 350)
TC gt 200mg/dl 15/40 37.5
238.9
Mean BNP 1376
TGs lt 200 32/40 80
137.2
Mean BNP 988
TGs gt 200 8/40 20
254
Mean BNP 1599.7
Data from file Reda et al 2003
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Abdominal obesity and not BMI
Body fat distribution not body weight
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CB1
Lipoprotein lipase activity
Adipose tissue
---
TNF-a
Adiponectin
Fat accumulation in adipose T
---
Adeponectin
----


----
FA oxidation
Glucose uptake
FFA clearance
Insulin sensetivity
Muscle
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• Blocking CB1 receptors can decrease
  intraabdominal obesity

• Oral cannabinoid therapy reduces progression of
  atherosclerosis

Activation of CB2 receptor may stop
atherosclerosis progression eg
TetraHydroCannabinol (THC) by stimulating CB2 in
mice
but
Smoking marijuana still bad for you!
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Blocking the over-activated endocannbinoid
system CB1 blockade
Central CB1 Blockade
Perepheral CB1 blockade (Adipose tissue)
Food intake
Eess abdominal fat
Adeponectin Insulin Resistence Alter
the atherogenic lipid profile CRP
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Changes in weight and waist size in the
rimonabant- and placebo-treated groups
End point Rimonabant 20 mg (n339) Placebo (n348) p
Weight (kg) -5.3 -1.4 lt0.001
Waist circumference (cm) -5.2 -1.9 lt0.001
Scheen A. American Diabetes Association 2005
Scientific Sessions June 10-14, 2005 San Diego,
CA.
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HDL cholesterol and triglyceride parameters in
the rimonabant- and placebo-treated groups
End point Rimonabant 20 mg (n339) Placebo (n348) Percent difference (compared with placebo) p
Change in HDL cholesterol (mg/dL) 6.6 2.7 8.4 lt0.001
Change in triglycerides (mg/dL) -31.2 3.6 16.4 lt0.001
Scheen A. American Diabetes Association 2005
Scientific Sessions June 10-14, 2005 San Diego,
CA.
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Visceral, subcutaneous fat linked to metabolic
syndrome, even in normal-weight individuals
Apr 11, 2005 Shelley Wood

• The association between higher visceral fat and
  metabolic syndrome was particularly noticeable in
  normal-weight and overweight men and women, but
  less so in the obese.

• Higher subcutaneous adipose tissue as well as
  higher intermuscular adipose tissue was
  significantly associated with metabolic syndrome
  in normal-weight and overweight, but not in
  obese, men, and not in women.

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CONCLUSIONS

• Describe the pathophysiology of intra-abdominal
  adiposity.
• Define the role of intra-abdominal adiposity as a
  major cause of cardiometabolic disease.
• Discuss current research related to CB1 blockade
  as a novel approach to cardiometabolic disease
  management.