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Metabolic syndrome is characterized by a large number of metabolic disorders, the findings being generally a combination of insulin resistance, obesity, hypertension, dislipidemia and pathological glucose tolerance or diabetes mellitus type II. Metabolic syndrome is diagnosed too seldom in view of the fact that a prevalence of at least 10% must be assumed for the population as a whole. Besides genetic predisposition, environmental factors such as diet, physical inactivity and nicotine and alcohol consumption play a decisive role in its clinical manifestation. The paper briefly examines the pathophysiological connections between the individual findings, with the central role of insulin resistance being emphasized. With a multifactorial therapy, in which non-medicamentous treatment is predominant, it must be assumed that on the whole compliance will tend to be poor. Prognostically the syndrome is serious, very frequently resulting in premature atherosclerosis. The paper concludes with a consideration of the underwriting of metabolic syndrome, one of the points being that the extramortality rates of the individual impairments should not be applied additively.

Insulin resistance caused by obesity and lack of physical activity plays a major role for the development of type 2 diabetes. If the reduced insulin action cannot be compensated by overproduction of insulin, glucose regulation disorder is developing. In addition, other trigger factors such as television viewing, sleep, alcohol or smoking are discussed. During the past years an intensification of pharmacological therapy was believed to be the major goal for the treatment of type 2 diabetes, now the value of nonpharmacological treatment improves. While in the past only nutrition was in the view of lifestyle research, recently a number of studies on the value of physical activity were published. In this paper an overview of recent studies showing the therapeutic potential of nonpharmacological therapies will be given. It will also be shown that these measures will not only optimize hyperglycaemia but also all other cardiovascular risk factors.

For the effective treatment of HIV infection, combinations of antiretroviral drugs that, at various points of attack, prevent viral replication are used. After the introduction of HIV-1 specific protease inhibitors, various metabolic complications and changes in body habitus manifesting as abnormal fat distribution were observed in HIV patients. These side effects, initially assigned class-specifically to the protease inhibitors, have, however, also been frequently seen under other drug combinations. Changes to body habitus as a result of fat redistribution have mostly been designated as lipodystrophy syndrome, but are now increasingly being recognized as highly heterogeneous abnormalities. Furthermore, the disturbances of glucose and fat metabolism may occur completely independently of phenotypic habitus changes. The result is that both the suspected pathophysiological relationships and the therapeutic consequences are becoming even more complex. This paper summarizes the current state of investigations into the side effects of antiretroviral therapy and their clinical consequences.

Non insulin dependent diabetes mellitus (NIDDM) and obesity are defined as classical insulin resistant states. Essential hypertension is now also considered to be an insulin resistant state, even in absence of NIDDM or obesity, as shown in epidemiological, clinical and experimental studies. Neither the underlying mechanism nor a direct causality between the two phenomena has been detected as yet, but different hypotheses have been postulated where, on the one hand, insulin resistance and hypertension are considered to be causally related and, on the other hand, they are considered to be parallel phenomena due to genetic and acquired factors. The clarification of the connection between hypertension and insulin resistance seems to be of great clinical importance, since they are both independent risk factors for cardiovascular disease and mortality from cardiovascular complications. This paper gives an overview of the results of recent research on the possible underlying pathogenetic mechanisms linking hypertension and insulin resistance.