The Metabolic Syndrome - A Postprandial Disease?

The last 50 years have witnessed a tsunami of a cluster of diseases - obesity, type 2 diabetes, hypertension and dyslipidemia - which are closely interrelated and strongly depend on environmental factors. After fifteen years of intensive pathophysiological clinical and epidemiological investigation, the metabolic syndrome paradigm was developed and first published in a comprehensive review in 1981 [1].

In 1999, the WHO published a preliminary proposal for the definition and - most important - cut-off limits for the components of the metabolic syndrome [2]. In the last few years, the definitions and cut-off limits have been adapted to recent developments in epidemiology [3], and the IDF tried to provide a unifying definition [4] giving rise to a controversial discussion on pathophysiology, relevance of traits and cut-off limits. Despite being an independent risk factor of cardiovascular disease, impaired glucose tolerance (IGT) was not included. Overnutrition and inadequate composition of food have been accepted as a driving force in the development of the metabolic syndrome, together with other environmental factors including socioeconomic conditions. Nowadays, the postprandial phase lasts about 18-20 hours a day, and it is no surprise that metabolic and hormonal regulation derangement start in the postprandial phase. Immune response to food and intestinal hormones play a central role in insulin secretion and insulin resistance. Excessive postprandial glucose excursion has harmful effects on the vessel wall endothelium via oxidative stress [5]. It has become increasingly evident that the metabolic syndrome starts as a postprandial disease. This was the reason for organizing the first international symposium on this burning issue, which took place in Dresden in April 2005. Extended abstracts from this top-level symposium have been published previously [6]. This supplement presents selected contributions of this symposium.

A new development in metabolic syndrome research dealing with neuroendocrine regulation is presented in two papers by Zepter et al. and one by Pliquett et al. in this issue. An impressive and pragmatic epidemiological approach to the metabolic syndrome has been presented by leading Chinese epidemiologists, Yang and Yang, also in this issue.

In the scope of genetic factors, variants in the adiponectin gene seem to be a pathogenetic relevant parameter (Schwarz 1, this issue). On the environmental, side metabolic learning and the adaptation of the intestine to nutrition and luminal factors may influence disease development (Schmitz & Langmann, this issue). In the clinical part of the current issue, Pistrosch et al. report about the effect of diurnal blood glucose excursions on HbA_1c in patients with type 2 diabetes (Pistrosch, this issue). Furthermore, the impact of low-glycemic index foods and their role in postprandial hyperglycemia is introduced by Slama in this issue. The most efficient way of managing the metabolic syndrome and its complications is to prevent it from developing in the first place. Early lifestyle and pharmacologic preventive strategies have yielded a 25-60% risk reduction, especially for diabetes, but an even more promising reduction of cardiovascular risk. Schwarz et al. report on the challenge to manage the implementation of prevention programs considering physiological aspects of the disease and practical requirements during implementation in their second contribution in this issue.

These contributions present new and exciting information on features of the metabolic syndrome connecting environment with endocrine regulation, supporting the hypothesis that the metabolic syndrome starts with abnormal postprandial regulation as a consequence of overnutrition and low physical activity in an environment of stress and social frustration.

References

• 1 Hanefeld M, Leonhardt W. Das metabolische Syndrom.  Dt Gesundh Wesen. 1981;  36 545-551
• 2 WHO Consultation. .Definition, diagnosis and classification of diabetes mellitus and its complications, Part 1: Diagnosis and classification of Diabetes mellitus. World Health Organisation, Geneva 1999: 1-59
• 3 NCEP Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults. . Executive summary of the third report of the National cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high cholesterol in adults (Adult treatment panel III).  JAMA. 2001;  285 2486-2497
• 4 Alberti KG, Zimmet P, Shaw J. IDF Epidemiology Task Force Consensus Group. The metabolic syndrome-a new worldwide definition.  Lancet. 2005;  366 1059-1062
• 5 Monnier L, Mas E, Ginet C, Michel F, Villon L, Cristol JP, Colette C. Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes.  JAMA. 2006;  295 1681-1687
• 6 , The Metabolic Syndrome-a postprandial disease. A satellite symposium of the 1st International Congress on Prediabetes and the Metabolic Syndrome. Diabetes and Stoffwechsel (Abstaktband) 2005;  1-64

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