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Contributo allo studio del meccanismo d'azione ipouricemizzante del benziodarone
Gli autori illustrano il loro contributo allo studio del meccanismo d'azione ipouricemizzante del benziodaron
Visceral obesity and metabolic syndrome
There is increasing evidence for the existence of a condition consisting of a cluster of metabolic disorders which include insulin resistance, alterations in glucose and lipid metabolism, increased blood pressure and visceral obesity. The metabolic syndrome is now the favoured definition of the cluster. Each single component of the cluster increases the cardiovascular risk, but the combination of factors is much more important. Insulin resistance is the most frequently associated factor to the singular components of the syndrome: most authors believe that it may be the common aetiological factor. However, visceral obesity seems to be the main driving factor by means of the increased production of free fatty acids whose activity, in turn, might interfere with the action of insulin. Some questions exist about the syndrome because of the frequent lack in the cluster of one of the factors. This does not mean that the missing factor does not belong to the syndrome, but only that it is not yet clinically evident. Weight gain has been shown to be a strong predictor of the metabolic syndrome. This aspect gives strength to treatment and prevention because it means that losing weight or stopping weight increase might reduce the risk of a future appearance of a factor that is still not evident. Interventions to treat visceral obesity by means of losing weight seem to be the most efficacious way to treat the metabolic syndrome thus improving the most widespread cardiovascular risk factor in western countries
Ultrastructural features of cultured mature adipocyte precursors from adipose tissue in multiple symmetriclipomatosis
An ultrastructural study of adipocyte precursors from epididymal fat pads of adult rats in culture
The benefits of modest weight loss in type II diabetes
Obesity increases the risk of developing type II diabetes. However, the link between the two remains unclear, although insulin resistance and visceral adiposity are dominant risk factors. A study with CT scanning confirmed that the degree of visceral adiposity had a significant positive correlation with insulinaemia, and was negatively associated with insulin sensitivity. A 48 month retrospective study in patients with type II diabetes, who had received dietary therapy, identified a 'responder' group in whom metabolic improvements accompanied weight loss. Preferential loss of visceral fat may be an important factor in these 'responders'. Patients losing > 6.9 kg (or at least 10% mean baseline body weight) have demonstrated significant improvements in their glucose, HbA1 and lipid profiles. Modest weight loss by patients with type II diabetes therefore improves glycaemic control, insulin sensitivity and cardiovascular risk factors; and the risk of developing long-term diabetes-related complications may also be reduced by such metabolic improvements
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