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Introduction

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INTRODUCTION
INTRODUCTION
H. Haller
Franz Volhard Clinic at the Max Delbrück
Center for Molecular Medicine, Virchow
Klinikum, Berlin, Germany
Diabetes mellitus is the single most
important risk factor worldwide for the
development of atherosclerosis. Patients
with insulin-dependent diabetes mellitus
(IDDM) tend to develop signs of chronic
vascular disease (CVD). Furthermore, most
patients with long-standing non-insulindependent diabetes mellitus (NIDDM)
show signs of coronary artery disease,
peripheral artery disease, and nephrosclerosis during their lifetime. The development of effective preventive therapies and
treatment for CVD is therefore important.
This will be aided by an understanding of
the underlying metabolic causes of CVD.
The close association between diabetes
mellitus and atherosclerosis makes it likely
that diabetes-associated metabolic disturbances are responsible for the development of CVD. Increased plasma glucose
levels and hyperlipidaemia are the obvious candidates. In patients with IDDM,
CCC 0742–3071/97/S300S5–01
 1997 by John Wiley & Sons, Ltd.
hyperglycaemia precedes the development of atherosclerosis by years to decades. However, this sequence of events
is not so obvious in patients with NIDDM.
In these patients, the diagnosis of vascular
disease is often paralleled by the discovery
of hyperglycaemia; atherosclerosis is commonly diagnosed even before the metabolic disturbances of diabetes mellitus
are discovered.
As both the metabolic alterations in
NIDDM and CVD begin insidiously and
develop slowly, it is of particular importance to investigate the relationship
between early stages of vascular disease
and the earliest changes in diabetes mellitus. The earliest metabolic manifestation
of NIDDM is the state known as impaired
glucose tolerance (IGT). In this state, the
absorption of glucose postprandially is
delayed due to decreased sensitivity to
insulin. Although fasting blood glucose
values return to normal levels between
meals, the increased postprandial plasma
glucose levels and lipid concentrations
may have a damaging effect on the vessel
wall and may therefore contribute to the
development of CVD. Measurement of
these postprandial changes may help to
assess cardiovascular risk and identify
specific factors associated with a risk of
developing NIDDM.
The papers in this supplement issue of
Diabetic Medicine are based on a workshop held in London in November 1996.
They discuss postprandial disturbances in
glucose and lipid metabolism in patients
with diabetes mellitus, and their relationship to vascular disease. Epidemiological
evidence for a relationship between IGT
and CVD is considered in the papers by
S.M. Haffner and M. Hanefeld, while
S.W. Coppack and G. Steiner analyse the
relationship between postprandial lipoproteins and diabetes. The papers of F. Karpe
and T.E. Willnow describe the formation
of the postprandial chylomicron remnant
and its relationship to coronary artery
disease. A third group of papers focus on
postprandial changes in plasma glucose
and their effects on the vessel wall. Finally,
H. Schuster discusses a new approach,
which could help to identify the genes
that confer a risk of CVD.
Further research is required to establish
precisely which aspect of vascular function and which postprandial circulating
factors should be measured in order
to test the hypotheses that postprandial
changes pose an inherent risk to selected
individuals. If this hypothesis can be
validated, full-scale intervention trials
should be initiated to establish whether
therapeutic interventions can reduce the
risk of atherosclerosis in high-risk patients.
S5
DIABETIC MEDICINE, 1997; 14: S5
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