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CONTROVERSIAS EN TORNO AL

SÍNDROME METABÓLICO

Dr. ÁLVARO HERMIDA AMEIJEIRAS

HOSPITAL CLÍNICO UNIVERSITARIO SANTIAGO

Banting lecture 1988. Role of insulin resistance in human disease.

Reaven GM.

Department of Medicine, Stanford University Medical Center, California.

ResistanceResistance toto insulininsulin -stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance(IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals withnormal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cellis able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannotbe achieved, grossgross decompensationdecompensation ofof glucoseglucose homeostasis homeostasis occursoccurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid(FFA) concentration. PatientsPatients withwith NIDDM are NIDDM are alsoalso resistantresistant toto insulininsulin suppressionsuppression ofof plasma FFA plasma FFA concentrationconcentration, butplasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. Ifhyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resultingincrease in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepaticglucose production are likely to lead to significant fasting hyperglycemia under these conditions. Althoughhyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, thiscompensatory response of the endocrine pancreas is not without its price. PatientsPatients withwith hypertensionhypertension, , treatedtreated ororuntreateduntreated, are , are insulininsulin resistantresistant, , hyperglycemichyperglycemic, , andand hyperinsulinemichyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when theyare fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance andhyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the threevariables may be a causal one

Diabetes. 1988 Dec;37(12):1595-607.

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SÍNDROME METABÓLICO

PRO-INFLAMACIÓNHIPERGLUCEMIA BASAL

OBESIDAD

PRO-COAGULACIÓN

RESISTENCIA INSULÍNICA

DISLIPEMIA

SÍNDROME METABÓLICO (OMS 99)

RESISTENCIA INSULÍNICA (DM II/IGT/IFG)+

(≥ 2 factores de riesgo)

Obesidad visceralÍndice cintura/cadera > 0.85 mujer (>0,9 hombre)

ó IMC > 30 kg/m2

DislipemiaTriglicéridos ≥ 150 mg/dl

ó HDL < 39 mg/dl mujer (< 35 mg/dl hombre)

TAS/TAD≥ 140/90

MicroalbuminuriaVEA ≥ 20 µgrs/min

ó cociente albúmina/creatinina ≥ 30 mgrs/g

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SÍNDROME METABÓLICO (ATP III 02)

El diagnóstico precisa ≥ 3 factores de riesgo

Glucemia ayunas

TAS/TAD

Triglicéridos

≥ 110 (≥100)mg/dl

≥ 130/85 mmHg

< 50 mg/dlMujer

< 40 mg/dlHombre

Colesterol HDL

≥ 150 mg/dl

> 98 cmsMujer

> 102 cmsHombre

Circunferencia cintura

SÍNDROME METABÓLICO (AACE 03)

1 FACTOR DE RIESGO:IMC≥25 ó circunferencia

cintura>102 cms(H);>88cms (M)

40 años

Sedentarismo

No caucasico

Antecedentes familiares de DM ó enf. C-V

Antecedentes personales de intolerancia a la glucosa ó

diabetes gestacional

Acantosis nigricans

Síndrome de ovario poliquístico

Hígado graso no alcohólico

2 PARÁMETROS:Triglicéridos > 150 mgrs/dl

Colesterol-HDL: <40 (H);< 50(M)

TAS/TAD≥130/85

Glucemia en ayunas: 110-125 mgrs/dl

Test sobrecarga oral glucosa: >140 mgrs/dl (2

horas)

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Lakka HM, et al. The metabolic syndrome and total andcardiovascular disease mortality in middle-aged men. JAMA.

2002; 288: 2709-2716.

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Ford E. et al. JAMA 2002 (287): 356-9.

Wong et al. Am J Cardiol. 2003; 91: 1421-26.

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PREVALENCIA SÍNDROME METABÓLICO EN ESPAÑA

Síndrome metabólico en población laboral. Plan de Prevención del Riesgo Cardiovascular IBERMUTUAMUR

0102030405060708090

100

<30 30-40 40-50 50-60 >60

No SMSM

N: 176314

PREVALENCIA SÍNDROME METABÓLICO EN ESPAÑA

N: 470/18350

05

101520253035404550

18-29 30-39 40-49 50-59 60-69 70-79 >80

MujerHombre

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SÍNDROME METABÓLICO: ETIOLOGÍA

RESISTENCIA INSULÍNICA

Stress oxidativo

Disfunción endotelial

Ateromatosis

López-Candales et al. J. Med. 2001;32:283-300.

HIPERCORTISOLEMIA

Stress crónico

Lipogénesis

Resistencia insulínica

Bjorntorp P. et al. Scand. Cardiovasc. J. 2001; 35:172-7.

SÍNDROME METABÓLICO: ETIOLOGÍA (II)

OBESIDAD

ILK-6; PCR; NEFA; PAI-1

Pro-inflamación/trombosis/resistencia insulínica

St-Onge M-P et al. Diabetes Care 2004; 27: 2222-28.

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SÍNDROME METABÓLICO: TRATAMIENTO

1_ MODIFICAR ESTILO VIDA

DIETA EJERCICIO

NO FUMAR

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Duncan et al. Diabetes care 2003;26:557-62

Katzmorzyk PT et al. Heritage study. Med Sci Sport 2003; 35:1703-09.

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SÍNDROME METABÓLICO: TRATAMIENTO

2_ RESISTENCIA INSULÍNICA

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SÍNDROME METABÓLICO: TRATAMIENTO

3_ DISLIPEMIA

< 160BAJO RIESGO: 0-1 factores riesgo

< 130 (opcional <100)ALTO RIESGO: ≥ 2 factores riesgo*

< 100 (opcional <70)MUY ALTO RIESGO: Coronariopatía y/o

equivalente de riesgo (diabetes)

OBJETIVO LDL (MG/DL)CATEGORÍA RIESGO

* Tabaquismo, HTA≥ 140/90, HDL<40,AF Coronariopatía precoz (<55 varon;< 65 mujer),edad (>45 varón;>55mujer)

Grundy SM, Cleeman JI, Merz CNB, et al. Implications of recent clinical trials for the National Cholesterol EducationProgram Adult Treatment Panel III guidelines. Circulation. 2004;110:227-239.

SÍNDROME METABÓLICO: TRATAMIENTO

4_ HIPERTENSIÓN

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SÍNDROME METABÓLICO: TRATAMIENTO

4_ ANTIAGREGACIÓN

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St-Onge M-P et al. Diabetes Care 2004; 27: 2222-28.

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