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بسم الله الرحمن الرحيم
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Metabolic syndrome
By Dr Amr Abdelmonem,MD.Assistant professor of cardiothoracic anesthesia ,surgical intensive care and clinical nutrition in faculty of medicine, Cairo universityMember of North American Association For The Study Of Obesity
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What is metabolic syndrome?
• Metabolic syndrome is a collection of health risks that increase the chance of developing heart disease, stroke, and diabetes.
• The condition is also known by other names including Syndrome X, insulin resistance syndrome, and dysmetabolic syndrome.
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What are these health risks?ATP III Guidelines WHO Guidelines
Abdominal Obesity
Waist Circumference Waist/Hip Ratio Men > 40 inches (102 CM) >0.90 Women > 35 inches (88 CM) >0.85
Other Variables Triglycerides 150 mg/dL 150 mg/dLHDL-Cholesterol Men < 40 mg/dL <35 mg/dL Women < 50 mg/dL <39 mg/dLBlood Pressure 130/ 85 mm Hg >140/>90 mm HgFasting Glucose 110 mg/dL 110 mg/dLWHO guidelines also include microalbuminuria (>20 µg/min or albumin:creatinine ratio >30 mg/g).
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The Pathogenesis of metabolic syndrome
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Environmental lifestyle-related factors:
When we eat ,our bodies break down the food into its basic components ( protein- carbohydrates- fat), and absorbs them into blood stream rise in blood sugar pancreas will release insulin moves sugar into cells either burned for energy or stored away as fat in fat cells or glycogen in liver and muscles
Years of dietery abuse in susceptible patients malfunctioning of insulin sensors hyperinsulinemia
Continued dietery abuse insulin sensors to sluggish insulin resistance
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Markers of insulin resistance :
Hypertriglyceridemia
HDL
Hypertension
Hyperinsulinemia (>15µu/ml) Marc C,et al. Obes Res.2005;13:703
Abdominal obesity
Hyperglycemia
Marjo etal , proven liver fat accumulation as an important marker Obes Res 2002; 10: 859
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It is now clear that an individual could be
insulin-resistant from one of two main reasons
1. he/she could be genetically resistant (like Reaven’s group) or
2. Could acquire the resistance by becoming obese
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Obesity
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Lets walk through the fat metabolism pathway and follow the flow of fat molecules:
Fat travels in the form of triglycerides at cells ezymatic breakdowen fatty acids enter the cells mitochondria breakdowen fat in order to enter mitochondria ,fats need carnitine
insulin inhibits Fat- carnitine shuttle system fats move back into blood
Glucagon accelerates this shuttle system
Muscle ,liver, kidney, lung, heart and other cells break down fat
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Two enzyme systems on the surface of fat cells regulated by insulin and glucagon
Insulin stimulates lipoprotein lipase that transports fatty acid into fat cells
Glucagon stimulates hormone sensitive lipase that releases the fat from fat cells into the blood
Although we cannot control lipoprotein lipase directly, we can control It indirectly by cotrolling the metabolic hormones ,insulin and glucagon
Fat cells merely store the fat molecules !
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DYSLIPIDEMIA
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Where does cholesterol come from?
80 % comes from the body itself , every cell in the body is capable of making its own cholesterol , most don’t and rely instead on that made in the liver and skin.
Cholesterol and triglycerides are insoluble in blood
Lipoproteins are envelops that enclose cholesterol and triglycerides Making them soluble in blood,so that they can be transported to tissues
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Sequence of events in the life of lipoproteins
Liver Makes and release VLDL
TRIGLYCERIDES WITH CHOLESTEROL
TRI AND CHOLES MATUREVLDL
TriglyceridesReleased to bloodAnd tissues
CholesterolBulk +tri LDL
HDL
Scavenges cholesterlFrom tissues carriesThrough bloodHands it off to
VLDL
More triglycerides release
Removed by liver
CholesteroLrich
LDL
Released to tissuesDeposited in coronary arteries
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When the level of cholesterol inside the cells falls LDL receptors Attach to the surfaces of the hepatic cells invaginate LDL cholesterol By endocytosis
Obese patients with insulin resistance have LDL receptors dysfunction
Cholesterol synthesis inside the cells depends on an enzyme named3- hydroxy-3 methyl-glutaryl-coenzyme A reductase
Couple of hormones affect the activity of the rate limiting enzymeHMG-CoA reductase
INSULIN AND GLUCAGON
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Hypertension
Data from NHANES III show that the (age – adjusted prevalence) Of high blood pressure increases progressively with higher levels Of BMI in men and women
High blood pressure is defined as
SBP 140 mm Hg or MBP 90 mm Hg or currently taking antihypertensives
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What is the etiology that connects obesity and hypertension?
Hyperinsulinemia and Insulin resistance
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Mechanism
1. Increased sodium retention
2. Increased sympathetic nervous system activity
3. Alteration in the mechanics of blood vessels
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Recently
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Type II Diabetes mellitus
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•The cells become resistant to insulin that even large amounts cant adequately move the sugar into cells
•Resistin is a protein secreted by fat cells as a signal from adipose tissue linking obesity to insulin resistance and type II diabetes Liese et al, Eur J Nutr.2001;40:282
•Increased White blood cell count is correlated with insulin resistance in diabetic obese females
Pannacciulli et al,Obes Res.2003;11:1232
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Coronary artery disease
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• Observational studies have shown that overweight,obesity, and VAT are directly related to cardiovascular risk factors
( cholesterol , LDL, triglycerides, hypertension, fibrinogen,hyperinsulinemia , HDL, plasminogen activator inhibitor )
RECENTLYComplement 3 and acute phase proteins is the immunological link between central obesity and CHD
The term "Syndrome X" refers to a heart condition where chest pain and electrocardiographic changes that suggest ischemic heart disease are present, but where there are no angiographic findings of coronary disease.
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Obesity and cardiac dysrhythmias(prolonged Q-T interval)
• Q-T interval is usually measured in lead II , and is corrected for heart rate .
• Q-Tc= measured Q-T square root of R-R interval• Prolonged Q-T interval reflects prolonged
repolarization of the ventricle• Proposed mechanism is increased SNS activity• Recent study had found that Prolonged Q-T
interval is associated with abnormal WHR ,higher levels of FFA and hyperinsulinemia in obese women .
• Wight loss leads to normalization of Q-Tc with attenuation of hyperinsulinemia
Esposito et al,Obes Res.2003;11:653-659
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Oxidant Stress
Imbalance
Between
Formation Of Reactive oxygen/nitrogen species (ROS/RNS)
And Antioxidants
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Pathologic stress Induces monocytes to release mediators
(TNF and interleukins 1-6-8) Activates PMNs
Release ROS(superoxide (O2·-), hydrogen
peroxide, hypochlorite, nitric oxide (NO), hydroxyl radical
Induce tissue injury by:1. damaging DNA2. Cross linking cellular proteins3. Peroxidation of membrane lipids • Diminishing membrane fluidity• Increasing membrane permeability
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Oxidant Stress and Obesity
•Adipocytes and preadipocytes have been identified as sources of inflammatory cytokines:
including TNF , interleukin (IL)1-ß, and IL-6.
•Stimuli capable of inducing cytokine release from adipocytes may include:
lipopolysaccharides, intracellular triglycerides, and catecholamines
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We could predict that:
•The accumulation of intracellular triglycerides or tissue adiposity promotes increased oxidant stress
•Therefore reduction of total body fat through diet and/or exercise may be an effective means of reducing systemic inflammation and oxidant stress.
Consistent with this prediction
Reductions in plasma markers of oxidant stress and in ROS generation by isolated leukocytes have been observed after 4 weeks of energy restriction and weight loss.
Dandona et al. J Clin Endocrinol Metab,2001; 86:355-363
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Good news
Physical activity •Decreases adipose derived inflammatory mediators •Activates signaling pathways that lead to increased synthesis of intracellular antioxidants and antioxidant enzymes and decreased ROS production Miyazaki et al, Eur Appl Physiol.2001; 84:1-6 Pischon et al, Obes Res.2003;11:1055
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A novel pathway to the manifestations of metabolic syndrome(2004)
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