Molecular basis of the obesity associated with Bardet–Biedl syndrome

Guo, Deng‐Fu; Rahmouni, Kamal

doi:10.1016/j.tem.2011.02.009

Cited by 63 publications

(81 citation statements)

References 85 publications

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“…26 Carriers of BBS do not appear to be at increased risk of hypertension or diabetes, 4,10 although conflicting evidence exists regarding the possible increased risk of obesity in carriers. 4,10,27,28 An increase in renal cancers and malformations, 29 as well as retinal dysfunction, 30 has been reported in obligate carriers.…”

Section: Clinical Overviewmentioning

confidence: 99%

“…Furthermore, progress in understanding the biological basis for obesity in mouse models may lead to targeted drug therapy for the management of obesity in BBS patients. 28,52 MANAGEMENT A multidisciplinary approach is required to effectively manage this pleiotropic condition. Although research is in progress, there is still no targeted treatment for BBS.…”

Section: Biology Of the Diseasementioning

confidence: 99%

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Bardet–Biedl syndrome

2012

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Section: Clinical Overviewmentioning

confidence: 99%

Section: Biology Of the Diseasementioning

confidence: 99%

Bardet–Biedl syndrome

2012

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“…2,23 The prevalence of this group of disorders is one in 13,500 to 160,000 individuals depending on geographic location. 24 Energy dysregulation is thought to arise from defective leptin activity.…”

Section: Syndromic Disordersmentioning

confidence: 99%

“…24 Energy dysregulation is thought to arise from defective leptin activity. 23 Classic features include early-onset obesity, cognitive impairment, delayed puberty, renal anomalies (calyceal clubbing, parenchymal cysts, vesicoureteral reflux, hydronephrosis), post-axial polydactyly, and rod-cone dystrophy. 25 Hearing loss, diabetes mellitus, and congenital heart disease may also occur.…”

Section: Syndromic Disordersmentioning

confidence: 99%

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Screening for Hormonal, Monogenic, and Syndromic Disorders in Obese Infants and Children

Mason¹,

Page²,

Balikcioglu³

2014

Pediatr Ann

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The prevalence of pediatric obesity in the United States is nearly 17%. Most cases are “exogenous”, resulting from excess energy intake relative to energy expenditure over a prolonged period of time. However, some cases of obesity are “endogenous”, associated with hormonal, genetic, or syndromic disorders such as hypothyroidism, Cushing’s syndrome, growth hormone deficiency, defective leptin signaling, mutations in the melanocortin 4 receptor, and Prader-Willi and Bardet-Biedl syndromes. This article reviews the hormonal, monogenic, and syndromic causes of childhood obesity and identifies critical features that distinguish “endogenous” obesity disorders from the more common exogenous obesity. Findings that raise suspicion for endogenous obesity include onset in infancy, lack of satiety, poor linear growth, dysmorphic features, and cognitive dysfunction. Selection and interpretation of appropriate laboratory tests and indications for subspecialist referral are also discussed.

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Obesity and gut–microbiota–brain axis: A narrative review

Asadi

Mehr

Mohamadi

et al. 2022

Clinical Laboratory Analysis

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Introduction Obesity is a major health problem that is associated with many physiological and mental disorders, such as diabetes, stroke, and depression. Gut microbiota has been affirmed to interact with various organs, including the brain. Intestinal microbiota and their metabolites might target the brain directly via vagal stimulation or indirectly through immune‐neuroendocrine mechanisms, and they can regulate metabolism, adiposity, homoeostasis and energy balance, and central appetite and food reward signaling, which together have crucial roles in obesity. Studies support the concept of bidirectional signaling within the gut–brain axis (GBA) in the pathophysiology of obesity, mediated by metabolic, endocrine, neural, and immune system mechanisms. Materials and methods Scopus, PubMed, Google Scholar, and Web of Science databases were searched to find relevant studies. Results The gut–brain axis (GBA), a bidirectional connection between the gut microbiota and brain, influences physiological function and behavior through three different pathways. Neural pathway mainly consists of the enteric nervous system (ENS) and vagus nerve. Endocrine pathway, however, affects the neuroendocrine system of the brain, particularly the hypothalamus–pituitary–adrenal (HPA) axis and immunological pathway. Several alterations in the gut microbiome can lead to obesity, by modulating metabolic pathways and eating behaviors of the host through GBA. Therefore, novel therapies targeting the gut microbiome, i.e., fecal microbiota transplantation and supplementation with probiotics and prebiotics, can be a potential treatment for obesity. Conclusion This study corroborates the effect of gut microbiome on physiological function and body weight. The results show that the gut microbiota is becoming a target for new antiobesity therapies.

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Molecular basis of the obesity associated with Bardet–Biedl syndrome

Cited by 63 publications

References 85 publications

Bardet–Biedl syndrome

Bardet–Biedl syndrome

Screening for Hormonal, Monogenic, and Syndromic Disorders in Obese Infants and Children

Obesity and gut–microbiota–brain axis: A narrative review

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