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eBook ISBN: This manual teaches students and practitioners how to assess health and disease from an energetic perspective. Naturopathic medicine and Polarity Therapy, the book uses case histories to illustrate the.
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Finally, MC5R may play a role in the secretion of exocrine glands figure 2 2. The MC4R is a amino acid protein encoded by a single exon gene localized in chromosome 18q22 4. It belongs to the family of seven transmembrane G-protein coupled receptors and transduces signal by coupling to the heterotrimeric Gs protein and activating adenylate cyclase. MC4R activation by natural or pharmacological agonists leads to a decrease in food intake. Its role in energy balance has been well demonstrated in mice 5. Since , systematic genetic evaluation of MC4R gene revealed that MC4R -linked obesity is the most prevalent form of oligogenic obesity identified to date.

They include frameshift, inframe deletion nonsense and missense mutations located throughout the MC4R gene. In addition, the frequency of such heterozygous carriers in non-obese controls or in the general population is about 10 fold lower than in the cohorts of obese patients 7,8. In contrast with rare monogenic obesities, even a meticulous clinical analysis does not easily detect obesity stemming from MC4R mutations because of the lack of additional obvious phenotypes.

In families with MC4R -linked obesity, obesity tends to have an autosomal dominant mode of transmission, but the penetrance of the disease can be incomplete and the clinical expression variable moderate to severe obesity underlying the role of the environment and other potentially modulating genetic factors 3,9, Homozygous or compound heterozygous carriers of MC4R mutations are very rare As expected from a dominant condition, obesity is developed earlier in life and is more severe than for heterozygous carriers, but it does not display any additional unrelated phenotypes.

In heterozygous MC4R mutations carriers, the onset and severity of obesity vary and are related to the severity of the functional alteration caused by the mutation. The phenotype of MC4R mutation carriers has been debated. Many authors agree on that MC4R mutations facilitate early onset obesity. MC4R mutations carriers display increased linear growth, in particular in the first five years of life 14 but appear to be taller as adults only in rare cases 15, This trend is often observed in overweight and obese children.

Assessment of body composition in these patients demonstrates increase in both fat and lean mass One study performed in English children with MC4R mutations, has suggested that bone mineral density and size increase This potential increase of bone density may be explained, at least in part, by a decrease in bone resorption, as illustrated by decreases in bone resorption markers in the serum of patients with MC4R homozygous and heterozygous mutations 17, Obese children carrying MC4R mutations have a marked hyperphagia that decreases with age, when compared to their siblings 14 , while in both children and adults, no evidence has been found for a decreased metabolic rate in these patients.

Adult MC4R mutation carriers do not have an increased prevalence of diabetes or other obesity complications 8. In UK children, fasting insulinemia was found to be significantly elevated in MC4R mutation carriers, particularly before the age of 10 years when compared to age, sex and BMI matched control This hyperinsulinemia has not consistently been observed in children 12, 13 and in adults 6, MC4R mutations were also associated to a reduced risk of hypertension Finally, with respect to endocrine function, hypothalamo-pituitary axis and reproductive axis 9,10, 14 as well as thyroid function are normal in MC4R mutation carriers.

The role of MC4R mutations in cases of human obesity relies on two main arguments based on the frequency of MC4R mutations in different populations and their in vitro functional consequences. Firstly, MC4R mutations are more abundant in obese populations. Secondly, investigating the molecular mechanisms by which loss of function mutations in MC4R cause obesity have suggested a panel of functional anomalies: abnormal MC4R membrane expression, defect to the agonist response, and disruption in the intracellular transport of this protein.

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Normally, after ligand binding, MC4R activation stimulates Gs protein, leading to a subsequent increase in cAMP levels; however, the production of intracellular cAMP in response to aMSH peptides demonstrated a broad heterogeneity in the activation of the different MC4R mutants in response to aMSH, ranging from normal or partial activation to a total absence in activation 6, 7, 9, The intracellular transport defect of the mutated receptor, by intracytoplasmic retention, has been described for the majority of MC4R mutations found in childhood obesity 22 , but also in adults 6,7.

This mechanism explains the impaired response to agonists. In addition, MC4R has a constitutive activity, meaning a basal activity not necessitating the presence of a ligand, for which agouti related peptide AGRP acts as an inverse agonist In the absence of the ligand, MC4R has an inhibitory action on food intake. The systematic study of basal activity of some mutations has shown that an alteration in this activity may be the only functional anomaly found, in particular for mutations located in the N-terminal extra-cytoplasmic part of the receptor A tonic satiety signal, provided by the constitutive activity of MC4R could be required in the long-term regulation of energy balance.

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It is accepted that MC4R mutations cause obesity by a haploinsufficiency mechanism rather than a dominant negative activity. While the roles of homo and hetero-dimerization in G protein synthesis and maturation are emphasized, some dominant negative effects of MC4R mutations might not be excluded.

To date, it is questionable to perform in routine systematic detection of MC4R mutations in obese subjects with a strong obesity familial history. Although knowing the biological reason ie: altered melanocortin pathway leading to an increased susceptibility to obesity might be of interest in some individuals, no specific therapeutic is still available and the severity of phenotype is highly variable within MC4R mutation carrier families.

It may however become necessary in few years in case of development of specifics drugs such as MC4R agonists in order to detect patients that may be eligible for such treatments To date, any specific management is necessary for MC4R mutation obese patients except for well-balanced diet and physical activity. However, interestingly, physical activity may have a specific role for modulating the obese phenotype in case of MC4R anomalies. It suggests its specific role in the management of MC4R mutation related obesity and possibly the prevention of weight gain in relatives with MC4R mutation.

In addition, due to its important role in obesity, MC4R is becoming an attractive candidate drug target suggesting that identification and design of ligands or peptides may rescue the phenotype of the particular molecular mechanistic defect. Several synthetic ligands from the classical NDP-MSH peptides to the multiple tetrapeptides and small molecule MC4R agonists have been in vitro tested with variable results 27, But, they have to face normal concerns of targeting GPCRs and specific difficulties of possible side effects due to the widespread expression of MC4R in the brain and the already demonstrated role of MC4R in erectile function 27, At long term, this type of treatment should be evaluated in heterozygous patients for MC4R mutations with impaired aMSH activity, in specific clinical investigation protocols in order to provide effective anti-obesity treatment probably in combination with other approaches such as diet and physical activity.

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Actually, novel pharmacological MC4R agonists have been tested in vitro and can restore a normal activity in mutated receptor and preclinical trials are performed No side effect, in particular in blood pressure or heart rate, was observed in this study Today, bariatric surgery is the only long-term efficient treatment for severe obesity 30 using several operative methods laparoscopic gastric bypass, gastric banding or sleeve gastrectomy. The question of such treatement and its potential efficiency is crucial in patients with genetic abnormalities previously described in this chapter.

Currently, data on bariatric surgery in patients with genetic obesity are limited and controversial. In 4 patients with heterozygous MC4R mutations, weight loss after Roux-en-Y gastric bypass surgery was identical to controls without MC4R mutations suggesting that heterozygous MC4R mutation status should not influence the decision to perform surgery Recent studies confirmed these findings in a group of obese adults 32, In contrast, in a teenager with complete MC4R loss of function, laparoscopic adjustable gastric banding resulted in the absence of long-term weight loss 12 months postoperatively suggesting that the full interruption of melanocortin pathway may not be counteracted by bariatric surgery Other studies on the effect of bariatric surgery in MC4R mutated patients are needed.

In humans, strong evidence of a causative role for MC3R mutations is still lacking. Several rare mutations with functional alterations have been described to be associated with severe obesity in children 36, In adults, some MC3R mutations, leading to amino-acid changes in the receptor, have been also described in a group of obese subjects 38 but the total prevalence of rare MC3R variants was not significantly different between cohorts of severely obese subjects and lean controls No specific phenotype of MC3R mutations has been identified. As linkage studies are concordant with the presence of a susceptibility gene for human obesity at the MC3R locus 20q Concerning management of patients carrying MC3R mutations, few data are available.

In a study, Santoro et al found that Thr6Lys and Val18Ile were associated with a differential weight loss in response to a negative energy balance in obese children In adults, in a randomised trial of hypoenergetic high vs low-fat diet, the presence of MC3R mutations did not impact on weight evolution To our knowledge, no data are available on the effect of bariatric surgery.

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The high frequency of MC4R mutation associated to obesity shows that they can be considered as the first cause of oligogenic obesity between the rare monogenic obesities leptin deficiency,.. The implication of MC3R in obesity is still debated and need to be confirmed. Development of MC4R agonists in close future may be the first example of personalized treatment in obesity and may limit indications of bariatric surgery in young people. Your email address will not be published.

Save my name, email, and website in this browser for the next time I comment. Leave this field empty. Select a page. Figure 2: Role of the 5 melanocotin receptors activated by peptides derived from the cleavage of the pro-opiomelanocortin POMC. References A. Harrold, G. Melanocortin-4 receptors, beta-MSH and leptin: key elements in the satiety pathway. Peptides ; Cone, RD.

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The Energetics of Health E-Book: A Naturopathic Assessment

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