Protected denomination of origin (PDO) cheeses have distinctive sensorial characteristics. They can be made only from raw milk possessing specific features, which is processed through the ‘art’ of the cheesemaker. In general, the distinctive sensorial traits of PDO cheese cannot be achieved under different environmental–production conditions for two main reasons: (1) some milk features are linked to specific animal production systems; (2) cheese ripening is affected by the interaction between milk (specific) and the traditional technology applied to the transformation process (non-specific). Also, the environment for a good ripening stage can be quite specific and not reproducible. With reference to milk, factors of typicality are species and/or breed, pedo–climatic conditions, animal management system and feeding. Other factors that influence cheese quality are milk treatments, milk processing and the ripening procedures. The technology applied to most cheeses currently known as PDO utilizes only raw milk, rennet and natural lactic acid bacteria, so that milk must be, at its origin, suitable for processing. The specific milk characteristics that ensure a high success rate for PDO cheeses are high protein content and good renneting properties, appropriate fat content with appropriate fatty acid composition and the presence of chemical flavours originating from local feeds. Moreover, an appropriate microflora is also of major importance. The factors that contribute to achieving milk suitable for transformation into PDO cheese are genetics, age, lactation stage, season and climate, general management and health conditions, milking and particularly feeding, which affect nutrient availability, endocrine response and health status, and also the presence of microbes and chemical substances which enrich or reduce the milk–cheese quality. Many of these factors are regulated by the Producer Associations. However, the secret of the success of PDO cheeses is the combination of modern technology and tradition, with the objective of adapting the product to market demand, without losing specificity, originality and authenticity.

During the past few years, there have been two major developments, if not revolutions, in the field of energy balance and weight regulation. The first at the molecular level, which was catalysed by developments in DNA screening technology together with the mapping of the human genome, has been the tremendous advances made in the identification of molecules that play a role in the control of food intake and metabolic rate. The second, at the systemic level, which centered upon the use of modern technologies or more robust analytical techniques for assessing human energy expenditure in response to starvation and overfeeding, has been the publication of several papers providing strong evidence that adaptive thermogenesis plays a much more important role in the regulation of body weight and body composition than previously thought. Within these same few years, several new members of the mitochondrial carrier protein family have been identified in a variety of tissues and organs. All apparently possess uncoupling properties in genetically-modified systems, with two of them (uncoupling protein (UCP) 2 and UCP3) being expressed in adipose tissues and skeletal muscles, which are generally recognised as important sites for variations in thermogenesis and/or in substrate oxidation. Considered as breakthrough discoveries, the cloning of these genes has generated considerable optimism for rapid advances in our molecular understanding of adaptive thermogenesis, and for the identification of new targets for pharmacological management of obesity and cachexia. The present paper traces first, from a historical perspective, the landmark events in the field of thermogenesis that led to the identification of these genes encoding candidate UCP, and then addresses the controversies and on-going debate about their physiological importance in adaptive thermogenesis, in lipid oxidation or in oxidative stress. The general conclusion is that UCP2 and UCP3 may have distinct primary functions, with UCP3 implicated in regulating the flux of lipid substrates across the mitochondria and UCP2 in the control of mitochondrial generation of reactive oxygen species. The distinct functions of these two UCP1 homologues have been incorporated in a conceptual model to illustrate how UCP2 and UCP3 may act in concert in the overall regulation of lipid oxidation concomitant to the prevention of lipid-induced oxidative damage.