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.The recently discovered peripheral hormone leptin, which is secreted bywhite adipocytes and is responsible for genetic obesity in the mouse, hasgained widespread interest in eating disorder pathophysiology, because it is apotent satiety factor and is involved in the fasting-induced inhibition of thegonadal axis [364].In particular, leptin behaves as a peripheral sensor of thebody fat mass: when adipose stores of the organism increase, leptin isproduced in larger amounts, which signals to the brain the need to reduce foodingestion and to increase energy expenditure.However, factors other thanadipocyte size and fat content, especially energy availability and the macromicronutrient composition of the diet, influence leptin production [364].Given this background, it is not surprising that in underweight peoplewith anorexia nervosa the plasma leptin levels are consistently reduced andcorrelate with patients BMI and body fat mass [365 368].During therecovery of body weight, a progressive increase in leptin concentrations isobserved in anorexic individuals [366].Furthermore, it has been shownthat, in anorexics undergoing nutritional treatment, a too rapid weight gain,which implies a substantial increase in circulating leptin, is associated witha poor prognosis [369].Because leptin is a satiety factor, this finding wouldsuggest that a too rapid increase of leptin production during nutritionalrehabilitation would result in a possible excessive suppression of appetiteand an enhanced energy expenditure that contrast with the therapeuticprocess.Finally, given the stimulatory role of leptin on the HPG axis, itsreduced production in anorexia nervosa could be involved in thedeterminism of menstrual alterations.In this regard, evidence has beenprovided that a critical leptin level is needed to maintain menstrual cyclicityin underweight women [370].In normal-weight subjects with bulimia nervosa, circulating leptin isreported to be either decreased or normal [253,367,368,371,372].Studiesshowing reduced leptin levels in bulimics indicate that this alteration wasnot related to changes in patients BMI or body fat mass [368,371,372].Moreover, leptin response to acute fasting is completely blocked insymptomatic bulimics [253].These results suggest that the deranged leptinphysiology in bulimia nervosa reflects changes in subjects nutritionalparameters and/or eating patterns rather than modifications of body fatmass.Because leptin behaves as a satiety factor, it is possible that its reducedproduction contributes to the binge eating behaviour of bulimics.Indeed,human laboratory studies suggest that bulimic patients have diminishedsatiety responses [6], that could be mediated by either a decreased tonicproduction of leptin or a lack of its adequate response to acute changes inthe energy intake. 166 ___________________________________________________________________________ EATING DISORDERSSUMMARYConsistent EvidenceIt is clear that in patients with eating disorders medical complications arevery common and usually occur as consequences of nutritional derange-ments secondary to the aberrant eating and abnormal compensatorybehaviours.In the most severe cases, impairments of peripheral organsand apparata represent a significant threat to the patient s life.In emaciatedanorexics, immediate risks come from starvation-induced cardiovascularand renal alterations, which may lead to the development of severearrhythmias and sudden death.Cardiovascular risks are increased in thosesubjects who vomit and/or abuse diuretics and laxatives, because of thesevere electrolytic perturbations that can follow these aberrant behaviours.In the longer term, underweight anorexics are exposed to consequences ofthe progressive impairment in bone density that increases the likelihood ofpathological fractures.There is consistent evidence in the literature thatbone alterations are linked to the hypoactivity of HPG and hypothalamicGH somatomedin axes and, in some individuals, to the increasedproduction of cortisol.Moreover, it is evident that in emaciated anorexicsthe impaired function of the reproductive axis and the reduced activity ofthe thyroid gland aim to preserve residual energy stores for vital functionsand reduce the basal metabolic needs of the organism [ Pobierz całość w formacie PDF ]
zanotowane.pl doc.pisz.pl pdf.pisz.pl agnieszka90.opx.pl
.The recently discovered peripheral hormone leptin, which is secreted bywhite adipocytes and is responsible for genetic obesity in the mouse, hasgained widespread interest in eating disorder pathophysiology, because it is apotent satiety factor and is involved in the fasting-induced inhibition of thegonadal axis [364].In particular, leptin behaves as a peripheral sensor of thebody fat mass: when adipose stores of the organism increase, leptin isproduced in larger amounts, which signals to the brain the need to reduce foodingestion and to increase energy expenditure.However, factors other thanadipocyte size and fat content, especially energy availability and the macromicronutrient composition of the diet, influence leptin production [364].Given this background, it is not surprising that in underweight peoplewith anorexia nervosa the plasma leptin levels are consistently reduced andcorrelate with patients BMI and body fat mass [365 368].During therecovery of body weight, a progressive increase in leptin concentrations isobserved in anorexic individuals [366].Furthermore, it has been shownthat, in anorexics undergoing nutritional treatment, a too rapid weight gain,which implies a substantial increase in circulating leptin, is associated witha poor prognosis [369].Because leptin is a satiety factor, this finding wouldsuggest that a too rapid increase of leptin production during nutritionalrehabilitation would result in a possible excessive suppression of appetiteand an enhanced energy expenditure that contrast with the therapeuticprocess.Finally, given the stimulatory role of leptin on the HPG axis, itsreduced production in anorexia nervosa could be involved in thedeterminism of menstrual alterations.In this regard, evidence has beenprovided that a critical leptin level is needed to maintain menstrual cyclicityin underweight women [370].In normal-weight subjects with bulimia nervosa, circulating leptin isreported to be either decreased or normal [253,367,368,371,372].Studiesshowing reduced leptin levels in bulimics indicate that this alteration wasnot related to changes in patients BMI or body fat mass [368,371,372].Moreover, leptin response to acute fasting is completely blocked insymptomatic bulimics [253].These results suggest that the deranged leptinphysiology in bulimia nervosa reflects changes in subjects nutritionalparameters and/or eating patterns rather than modifications of body fatmass.Because leptin behaves as a satiety factor, it is possible that its reducedproduction contributes to the binge eating behaviour of bulimics.Indeed,human laboratory studies suggest that bulimic patients have diminishedsatiety responses [6], that could be mediated by either a decreased tonicproduction of leptin or a lack of its adequate response to acute changes inthe energy intake. 166 ___________________________________________________________________________ EATING DISORDERSSUMMARYConsistent EvidenceIt is clear that in patients with eating disorders medical complications arevery common and usually occur as consequences of nutritional derange-ments secondary to the aberrant eating and abnormal compensatorybehaviours.In the most severe cases, impairments of peripheral organsand apparata represent a significant threat to the patient s life.In emaciatedanorexics, immediate risks come from starvation-induced cardiovascularand renal alterations, which may lead to the development of severearrhythmias and sudden death.Cardiovascular risks are increased in thosesubjects who vomit and/or abuse diuretics and laxatives, because of thesevere electrolytic perturbations that can follow these aberrant behaviours.In the longer term, underweight anorexics are exposed to consequences ofthe progressive impairment in bone density that increases the likelihood ofpathological fractures.There is consistent evidence in the literature thatbone alterations are linked to the hypoactivity of HPG and hypothalamicGH somatomedin axes and, in some individuals, to the increasedproduction of cortisol.Moreover, it is evident that in emaciated anorexicsthe impaired function of the reproductive axis and the reduced activity ofthe thyroid gland aim to preserve residual energy stores for vital functionsand reduce the basal metabolic needs of the organism [ Pobierz całość w formacie PDF ]