Brain effects of melanocortins☆

Bertolini, Alfio; Tacchi, Raffaella; Vergoni, Anna Valeria

doi:10.1016/j.phrs.2008.10.005

Cited by 91 publications

(57 citation statements)

References 488 publications

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“…The melanocortins have a wide variety of effects in the brain (Bertolini et al, 2009). Proteolytic cleavage of the precursor pro-opiomelanocortin gives rise to several peptides, including adrenocorticotropin and ␣-MSH, both of which have been associated with erectile responses.…”

Section: G Adrenocorticotropin and Related Peptidesmentioning

confidence: 99%

Mechanisms of Penile Erection and Basis for Pharmacological Treatment of Erectile Dysfunction

2011

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Section: G Adrenocorticotropin and Related Peptidesmentioning

confidence: 99%

Mechanisms of Penile Erection and Basis for Pharmacological Treatment of Erectile Dysfunction

2011

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“…Exogenous melanocortins may markedly influence the behavior, although the role of endogenous melanocortins is doubtful in this respect (Bertolini et al 2009). These extra-adrenal effects of ACTH are worth to consider not only for research purposes, but also during the increasing number of diagnostic and therapeutic usage of ACTH, e.g., infant spasm (Mikati et al 2002), epilepsy (Gayatri et al 2007), and lipid-lowering activity (Thorisdottir et al 2009).…”

Section: Acth-independent Regulation Of the Corticosterone Secretionmentioning

confidence: 99%

The Vasopressin-Deficient Brattleboro Rat: Lessons for the Hypothalamo–Pituitary–Adrenal Axis Regulation

et al. 2012

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Adaptation to stress is indispensable to life and the hypothalamo-pituitary-adrenocortical axis is one of the major components of the adaptation. The hypothalamic component consists of corticotropin-releasing hormone and arginine vasopressin, with a questionable contribution of the latter. Vasopressin was more important in the regulation of the adrenocorticotropin secretion in the perinatal vasopressin-deficient Brattleboro rats than in adulthood, where its role depended on the nature of the stressor encountered. In adults, the vasopressin deficiency did not influence the development of chronic stress response. In the neonatal rats, the role of vasopressin was supported by the inhibitory action of a V1b antagonist and vasopressin antiserum. As the corticosterone response to stress did not follow the adrenocorticotropin levels, we assume the presence of an adrenocorticotropin independent adrenal gland regulation in the neonates. We have shown that the apparent dissociation of the corticosterone and adrenocorticotropin responses is not due to the different time course of the two hormone responses, to different level of the corticosterone binding globulin or to changes in the adrenal gland sensitivity. In vitro experiments point to the contribution of beta-adrenoceptors in the process. It was also confirmed by in vivo tests using the vasopressin-deficient Brattleboro pup as a model organism, where corticosterone levels may rise without adrenocorticotropin level changes. Another important question is the role of adrenocorticotropin beyond the corticosterone secretion regulation, which could be supposed, e.g., in cardiovascular events, immunological processes, and metabolism. We can conclude that Brattleboro rats gave us much information about the stress-axis regulation far beyond the role of vasopressin itself.

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“…MC4 activity affects meal size and meal choice, but not meal frequency. The type of diet also affects the efficacy of MC4 agonists to reduce food intake in rats [15,49,50].…”

Section: Melanocortin Mc-4 Receptor Agonistsmentioning

confidence: 99%

“…A number of groups have looked at the development of selective agonists for MC4 as potential treatments for obesity. However, the lack of suitable small-molecularweight nonpeptide agonist ligands or adverse events have limited clinical development of this target [15,49,50].…”

Section: Melanocortin Mc-4 Receptor Agonistsmentioning

confidence: 99%

New central targets for the treatment of obesity

Sargent

Moore

2009

Brit J Clinical Pharma

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The review focuses on the central neuronal circuits involved in energy homeostasis and the opportunities these offer for pharmacological intervention to decrease feeding behaviour and reduce weight. This article is based on the presentation 'New central targets for the treatment of obesity ' (Sargent, British Pharmacological society, Clinical Section Symposium, December 2008). Central neuronal substrates controlling weight offer numerous opportunities for pharmacological intervention. These opportunities range from non-specific enhancement of monoamine signalling (triple reuptake inhibitors) to targeting specific monoamine receptor subtypes (5-HT2c and 5-HT6). The data reviewed suggest that these approaches will lead to weight loss; whether this is sufficient to produce clinically meaningful effect remains to be determined. Combination therapy targeting more than one mechanism may be a means of increasing the magnitude of the response. Preclinical studies also suggest that novel approaches targeting specific neuronal pathways within the hypothalamus, e.g. MCH1 receptor antagonism, offer an opportunity for weight reduction. However, these approaches are at an early stage and clinical studies will be needed to determine if these novel approaches lead to clinically meaningful weight loss and improvements in co-morbid conditions such as diabetes and cardiovascular disorders. The obesity problemObesity is a major global health problem and rates of obesity [body mass index (BMI) >30 kg m -2 ] have risen steadily year on year. Recent figures show an incidence of obesity of more than 1 in 4 in many parts of the USA [1]. These high rates are similar in other developed countries and the incidence of weight gain is increasing in less developed regions. Obesity is not just a cosmetic or lifestyle illness but leads to many life-threatening health complications. As the BMI increases the incidence of metabolic disorders (Type 2 diabetes), hypertension, cancer and musculoskeletal problems increases [1][2][3]. In 1999, Calle et al. reported mortality rates for all causes doubled when the BMI increased from 25 to >35 [4].The annual direct healthcare costs associated with obesity in the USA are in excess of $93 billion [5]. Particularly worrying is the fact that the incidence of obesity in children and young adults is on the increase, with some reports suggesting that up to 25% of children may be obese. The long-term health implications of these findings are far reaching and suggest that for the first time intergenerational increase in life expectancy will not occur and these children will have a shorter life span than their parents because of health complications associated with weight gain [6] (Figure 1).Obesity occurs when the balance between energy input (food intake) and energy expenditure (exercise, activity) is disrupted, i.e. more food is consumed than utilized, leading to excess fat stores being laid down. Although for some people a calorie-restricted diet and exercise can lead to a reduction in weight gain, for many peop...

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Brain effects of melanocortins☆

Cited by 91 publications

References 488 publications

Mechanisms of Penile Erection and Basis for Pharmacological Treatment of Erectile Dysfunction

Mechanisms of Penile Erection and Basis for Pharmacological Treatment of Erectile Dysfunction

The Vasopressin-Deficient Brattleboro Rat: Lessons for the Hypothalamo–Pituitary–Adrenal Axis Regulation

New central targets for the treatment of obesity

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