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En
honor a los Profesores Gregorio Marañón
y Eskyl Kylin
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Presidentes: Prof.
A. García García y A. Ruiz-Torres
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| MADRID, 22 y 23 de Noviembre,
de 2002 Hospital de la Princesa. Madrid
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| Viernes,
22 de Noviembre de 2002 |
| 8:00 - 8:30 |
Recogida de Acreditaciones |
| 8:30 - 9:00 |
Apertura y bienvenida:
-Excma. Sra. Dña. Ana Pastor.
Ministra de Sanidad y Consumo
-Prof. A. Schüller. Presidente
de la Real Academia de Medicina y
Presidente de la Fundación Gregorio Marañón
-D. J. Gómez Zamora. Gerente
Hospital de La Princesa
-Dr. J. A. Gutiérrez Fuentes.
Dir. Fundación Lilly
Prof. A. Ruiz Torres: Porqué del Simposio |
| Mesa 1 |
Moderador : Dr. I. Ruipérez |
| 9:10 - 9:40 |
Gregorio Marañón, a relevant
personality in the history of Spanish Medicine
Dr. P. Nilsson
Reconocido como figura cumbre en el horizonte
intelectual del siglo XX en España, Gregorio
Marañón realizó una contribución notable a la
medicina y las humanidades. Después de breves
comentarios sobre el currículo marañoniano se
analizarán las cuatro etapas de su vida (1909-1922-1936-1943-1960)
para descubrir la continuidad y congruencia
en su vida y obra, a pesar de los periodos históricos
tan difíciles que le tocó vivir. Finalmente,
se exponen los principales capítulos de la Obra
médica de Marañón. |
| 9:40 - 10:10 |
Eskyl
Kylin, a short summary of his research on hypertension
and the Metabolic syndrome in the 1920's.
Prof. A. Fernández de Molina
The Swedish physician Eskil Kylin (1889-1975)
published already in 1923 a review on the Metabolic
syndrome, including aspects of hypertension,
hyperglycaemia and hyperuricaemia. In other
scientific works he described aspects of essential
hypertension in association with calcium metabolism
and influence of adrenaline on haemodynamics
and glucose metabolism. Therefore it is of interest
to further study his ways of thinking and doing
experimental medicine, in order to increase
the knowledge about the medical history of the
Metabolic syndrome based on insulin resistance.
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| 10:15 - 10:45 |
Café |
| Mesa 2 |
Moderadora : Dra. M. García
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10:45 - 11:15
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Insulin resistance and
cardiovascular disease - the Uppsala studies
Prof. H. Lithell
In Uppsala, Sweden, a cohort study started in
1970 with a health survey of 2300 men. They
have then been invited every 10 years. Annual
checks of the official cause of death registry
have been made. During almost 30 years follow-up
insulin resistance was an independent and strong
risk factor for coronary heart disease. Diet,
physical exercise and anti-hypertensive treatment
are environmental factors that influence insulin
resistance. |
| 10' |
Discusión |
11:30 - 12:00
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The
Metabolic syndrome in Spain
Prof. M. Serrano Ríos
The term Metabolic syndrome refer to a collection
of "clusters" of metabolic (DM/IGT, visceral
obesity, dislypidemia, hyperuricemia), nonmetabolic
(high blood pressure, altered coagulation/fibrinolysis),
and proinflammatory markers (CRP, IL-6), conferring
high cardiovascular risk/morbidity/mortality;
insulin resistance being often a link between
those "clusters". The etiology is multifactorial,
polygenes/environmental factors (diet, physical
activity, smoking, alcohol intake). Several
criteria are used for definition. In Spain,
R. Gabriel, M. Serrano Rios, et al, using OMS/EGIR
criteria have reported an overall prevalence
similar to other European countries (15.5/19%).
A crossectional population based study of MS
(ATPIII/criteria) conducted in the Castilian
province of Segovia is reported and commented.
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| 10' |
Discusión |
12:15 - 12:45
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Genetics of the Metabolic
syndrome
Prof .L. Groop
Several single nucleotide polymorphisms (SNPs)
or combinations of them (haplotypes) have been
identified in type 2 diabetic individuals in
genes encoding for the beta-2 and beta-3-adrenerigc
receptors, calpain 10, skeletal muscle glycogen
synthase (GYS1), PPARg, sulfonylurea receptor
(SUR) etc. For other genes like adiponectin
or the uncoupling proteins, the association
has been with obesity or the Metabolic syndrome
rather than with type 2 diabetes. However, each
of these genes contributes only a small proportion
to the individual and population risk of type
2 diabetes and this contribution seems to differ
among different parts of the world. The population
attributable risk for the Pro12Ala polymorphism
in the PPARg gene is about 20 %, whereas for
the calpain 10 haplotype is 14% in Mexican Americans,
but only 4% in Europeans. More importantly,
the risk is further influenced by environmental
factors like diet (PPARg ) or excercise (GYS1). |
| 10' |
Discusión |
| 13:30 |
Almuerzo |
| Mesa 3 |
Moderador : C. Sánchez
Ferrer |
15:30 - 16:00
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Insulin Resistance and
the Metabolic syndrome: lessons from transgenic
animal models
Prof. Fátima Bosch
La diabetes tipo 2 está asociada a alteraciones
patofisiológicas complejas y es difícil determinar
que defectos son primarios y cuales consecuencias
secundarias de los cambios metabólicos. En nuestro
laboratorio estamos estudiando, en animales
transgénicos que sobrexpresen enzimas claves
en el control de las vías metabólicas (GK y
PEPCK), el papel del tejido adiposo, músculo
esquelético y células ß en el desarrollo de
resistencia a la insulina y a la obesidad. Los
resultados obtenidos en estos modelos serán
discutidos. |
| 10' |
Discusión |
16:15 - 16:45
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Magnesium and calcium homeostasis
in insulin resistance and the Metabolic syndrome
Dr. A.Hänni
During the hyperinsulinemic euglycemic clamp
test the changes in circulating mineral status
are correlated to alterations in blood pressure.
A more pronounced increase in the circulating
ionized calcium and magnesium concentrations
was related to a greater blood pressure decline.
Both body mass index and insulin-mediated glucose
disposal, were correlated to the changes in
serum aldosterone concentration during the hyperinsulinemia. |
| 10' |
Discusión |
| 17:00 - 17:30 |
Café |
17:30 - 18:00
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Tissue-specific role of
IRS-s in the insulin resistance syndrome
Prof. M. Benito
Type-2 diabetes is a polygenic disease based
on a defect in the peripheral insulin action
and also a pancreatic insulin secretion deficiency.
Insulin resistance in peripheral tissues such
as skeletal muscle, adipose tissues and liver
is the most important feature of pre-diabetic
states. To study the insulin action and inaction,
several monogenic and polygenic mouse models
carrying nulls mutations on insulin resistant
genes such as insulin receptor, IRSs, Glut-4,
Glucokinase have been developed. In addition,
using such models we obtained to new cellular
lines to study the role of IRSs in the tissue-specificity
of insulin action and resistance. |
| 10' |
Discusión |
18:15 - 18:45
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Non
metabolic effects of insulin on the vascular
tissue
Dr. D. Vicent
Vascular complications are the major cause of
mortality and morbidity in diabetes mellitus
and other insulin resistant conditions. Experiments
in cell cultured models have revealed that insulin
effects in vascular tissues can be both, protective
and deleterious. The generation of an endothelial
cell-specific insulin receptor knockout mouse
has revealed that, even though insulin is not
a central regulator of vascular function, it
plays an important role in vascular biology. |
| 10' |
Discusión |
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| Viernes,
22 de Noviembre de 2002 |
| Mesa 4 |
Moderador : Prof. A. Schüller |
9:30 - 10:00
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Neuroendocrine alterations
in the Metabolic syndrome
Dr. P. Nilsson
Neuroendocrine aspects of the Metabolic syndrome
are becoming increasingly important in the understanding
of its pathophysiology. Recent studies have
indicated that disturbances in cortisol metabolism,
gonadal sex hormone regulation, and sympathetic
nervous activity have all been associated with
the Metabolic syndrome. Even fetal programming
could possibly influence stress susceptibility
and neuroendocrine function. This new understanding
could hopefully give new opportunities for treatment
possibilities in the future. |
| 10' |
Discusión |
10:15 - 10:45
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Endothelial dysfunction
in diabetes and Metabolic syndrome
Dr. L. Rodríguez Mañas
En el diabético, la disfunción endotelial se
asocia a la enfermedad y, más concretamente,
a mecanismos ligados a la hiperglucemia, entre
los que cabe destacar los debidos a la glicación
no enzimática de proteínas. Aunque tradicionalmente
se ha prestado mayor atención a los productos
terminales (AGEs), los productos de Amadori,
incluyendo la glicohemoglobina, parecen desempeñar
también un papel relevante. |
| 10' |
Discusión |
| 11:00 - 11:30 |
Café |
11:30 -12:00
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Metabolic syndrome and
coronary heart disease
Prof. P. González Santos
Independientemente de la gran capacidad aterogénica
de la DM tipo 2, en los últimos años se ha comprobado
que la resistencia a la insulina y la hiperinsulinemia,
en ausencia de diabetes, tienen un papel destacado
en la patogenia de la enfermedad coronaria,
habiéndose encontrado una correlación positiva
en algunos estudios prospectivos. El riesgo
está condicionado por la asociación con HTA,
obesidad central, alteraciones trombogénicas
y, sobre todo, hipertrigliceridemia y alteraciones
lipoprotéicas. |
| 10' |
Discusión |
12:15 - 12:45
| Lipid
treatment of the Metabolic syndrome, example
from the Scandinavian Simvastatin Survival Study
Prof. A. G. Olsson
Plasma lipid abnormalities of the Metabolic
syndrome include high plasma triglyceride, low
HDL cholesterol concentrations and increased
levels of small dense LDL. The 4S investigated
if treatment of patients with coronary heart
disease and increased cholesterol concentration
with 20-40 mg of simvastatin could prolong life.
Results showed that patients with elevated LDL-C,
low HDL-C, and elevated triglycerides were more
likely than patients with isolated LDL-C elevation
to have other characteristics of the Metabolic
syndrome, had increased risk for CHD events
on placebo, and received greater benefit with
the statin therapy. |
| 10' |
Discusión |
| 13:00 -13:30 |
Dr.
R. Carraro: Comentarios y conclusiones
Prof. A. García García: Despedida
Dr. J. A. Gutiérrez Fuentes: Agradecimientos
y despedida |
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| PROMOTORES |
Instituto
Universitario de Investigación Gerontológica y Metabólica.
Hospital Universitario de la Princesa.UAM
Fundación Teófilo Hernando
Fundación Gregorio Marañón
Fundación Lilly |
| PATROCINIO |
Fundación
Lilly |
| COMITÉ
CIENTÍFICO Y ORGANIZADOR |
F. Abad
R. Carraro
A. García García
J. García Mayordomo
M. García
J. A. Gutiérrez Fuentes
Y. Martín
A. Ruiz Torres |
| LUGAR
DE CELEBRACIÓN DEL SIMPOSIO |
Hospital
Universitario de la Princesa (salón de actos)
Calle Diego de León, 62. 28006 - MADRID |
| INFORMACIÓN |
http://www.fundacionlilly.com/ |
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