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Adult endocrinology

Insulin Resistance & The Many Faces Of The Metabolic Syndrome

We welcome you to a selection of talks from the live sympsoium titled "Metabolic Syndrome / Metabolic Risks: Implications for Diabetes and Cardiovascular Risk Reduction." The live program addressed the basic underlying genetic, molecular and pathophysiologic mechanisms of the metabolic syndrome/metabolic risks.

We are honored to present to you many world leaders in science. A unique group of basic and clinical experts in the biology of lipid and glucose metabolism presenting their work and discussing the challenges of translating scientific knowledge into practical applications in medicine.

Description of Dr. Reaven's presentation: An enormous amount of new information relevant to the role of insulin resistance in human disease has appeared since the introduction of the concept of Syndrome X and understanding of the clinical implications of insulin resistance and its consequences have evolved. The goal of this presentation is to: 1) briefly review the clinical abnormalities that occur in insulin resistant persons; and 2) evaluate the relationship between insulin resistance and the component parts of the various definitions of the Metabolic Syndrome.

When is a cluster a cluster?

Description of Dr. Yudkin's presentation: The Metabolic Syndrome has been defined mainly on the basis of epidemiological data. Dr. Yudkin suggests, however, that epidemiology has several pitfalls which make it necessary to use other additional methods to look at causation. The definition of Syndrome X as an association between glucose intolerance, dyslipidaemia, hypertension and insulin resistance, was based on small numbers of hypertensive subjects in whom ‘clustering’ was observed. Dr. Yudkin argues that little evidence exists that the Metabolic Syndrome is caused by insulin resistance. He suggests that fat in the abdomen, liver, muscles and around vessels provides the common antecedent linking insulin resistance to vascular disease.

The Mitochondrial Hypothesis & Diabetes Pathogenesis

Description of Dr. Patti's presentation: Recent genomic, ultrastructural, and functional analyses have supported an emerging paradigm that both insulin resistance and diabetes are associated with defects in mitochondrial function and/or expression of nuclear-encoded mitochondrial genes in skeletal muscle. Patti and colleagues evaluated gene expression phenotypes as a function of genotype and diabetes risk factors. Their data indicate mitochondrial gene expression may be modulated by both genetic background and insulin resistance, while obesity-linked environmental risk factors can further modify oxidative and mitochondrial gene expression via reductions in PGC1-dependent transcription.

CNS Regulation Of Insulin Resistance

Description of Dr. Schwartz's presentation: Through their central actions on food intake and energy expenditure, the hormones insulin and leptin, which circulate at levels proportional to body fat mass, promote weight stability as part of an ‘adiposity negative feedback’ control system. Among several brain areas that transduce input from insulin and leptin into behavioural and metabolic responses is the hypothalamic arcuate nucleus. Dr. Schwartz summarizes the data that suggest that hypothalamic integration of adiposity signals is essential to the regulation of both body fat mass and blood glucose levels, and that defects in this control system may therefore contribute to the link between obesity and type 2 diabetes.

Impact Of Exercise & AMPK On Inflammation & Insulin Action

Description of Dr. Ruderman's presentation: It has long been appreciated that exercise enhances insulin sensitivity in humans and that when performed regularly it decreases the risk for type 2 diabetes and coronary heart disease. Dr. Ruderman reviews recent studies that suggest that these effects are mediated by the fuel-sensing enzyme AMP-activated protein kinase (AMPK). An increasing body of evidence has linked the metabolic syndrome to altered lipid metabolism, mitochondrial dysfunction and a pro-inflammatory state. Studies in rodents suggest that many if not all of these abnormalities may be attributable to dysregulation of AMPK. It remains to be determined if AMPK is similarly linked to the metabolic syndrome in humans. Dr. Ruderman states, however, that the efficacy of exercise, caloric restriction, metformin and the Tzds in treating and preventing insulin resistance and associated disorders in humans suggests this is likely.

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