Obesity induces resistance to central action of BMP8B through a mechanism involving the BBSome

Rial-Pensado, Eva; Freire-Agulleiro, Oscar; Rios, M Serrano; Guo, Deng Fu; Contreras, Cristina; Seoane-Collazo, Patricia; Tovar, Sulay; Nogueiras, Rubén; Diéguez, Carlos; Rahmouni, Kamal; López, Miguel

doi:10.1016/j.molmet.2022.101465

Cited by 7 publications

(6 citation statements)

References 47 publications

(151 reference statements)

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“…46 The BBSome has been implicated in its central action as mice with missense disease-causing mutations in the Bbs1 gene are resistant to the effects of centrally administered BMP8B. 47 A limited number of studies with small numbers of patients and control subjects have examined levels of other peptide hormones that are important for appetite control and the regulation of metabolic phenotype. No significant differences in ghrelin, glucagon-like peptide-1 (GLP-1), or adiponectin levels have been shown in patients with BBS.…”

Section: Bardet-biedl Syndrome and Other Neuropeptidesmentioning

confidence: 99%

“…It has both peripheral as well as central actions within the ventromedial hypothalamus to regulate energy homeostasis by modulating brown adipose tissue thermogenesis and white adipose tissue browning 46 . The BBSome has been implicated in its central action as mice with missense disease‐causing mutations in the Bbs1 gene are resistant to the effects of centrally administered BMP8B 47 …”

Section: Mechanisms Of Metabolic Dysfunction In Bardet‐biedl Syndromementioning

confidence: 99%

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Bardet‐Biedl syndrome: A focus on genetics, mechanisms and metabolic dysfunction

Tomlinson

2024

Diabetes Obesity Metabolism

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Bardet‐Biedl syndrome (BBS) is a rare, monogenic, multisystem disorder characterized by retinal dystrophy, renal abnormalities, polydactyly, learning disabilities, as well as metabolic dysfunction, including obesity and an increased risk of type 2 diabetes. It is a primary ciliopathy, and causative mutations in more than 25 different genes have been described. Multiple cellular mechanisms contribute to the development of the metabolic phenotype associated with BBS, including hyperphagia as a consequence of altered hypothalamic appetite signalling as well as alterations in adipocyte biology promoting adipocyte proliferation and adipogenesis. Within this review, we describe in detail the metabolic phenotype associated with BBS and discuss the mechanisms that drive its evolution. In addition, we review current approaches to the metabolic management of patients with BBS, including the use of weight loss medications and bariatric surgery. Finally, we evaluate the potential of targeting hypothalamic appetite signalling to limit hyperphagia and induce clinically significant weight loss.

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Section: Bardet-biedl Syndrome and Other Neuropeptidesmentioning

confidence: 99%

Section: Mechanisms Of Metabolic Dysfunction In Bardet‐biedl Syndromementioning

confidence: 99%

Bardet‐Biedl syndrome: A focus on genetics, mechanisms and metabolic dysfunction

Tomlinson

2024

Diabetes Obesity Metabolism

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“…The selection of these doses was based on previous reports (López et al, 2010;Martinez-Sanchez et al, 2017a;Martínez-Sánchez et al, 2017). The osmotic minipumps were inserted in a subcutaneous pocket on the interscapular surface created using blunt dissection (Martins et al, 2016;Martinez-Sanchez et al, 2017a; Frontiers in Physiology frontiersin.org Martínez-Sánchez et al, 2017;Rial-Pensado et al, 2022). The correct position of the cannuale was verified by histological examination of coronal sections of the brains, as shown (López et al, 2010;Martínez de Morentin et al, 2014;Martins et al, 2016;Martínez-Sánchez et al, 2017).…”

Section: Stereotaxic Microinjection Of T3mentioning

confidence: 99%

Temperature modulates systemic and central actions of thyroid hormones on BAT thermogenesis

et al. 2022

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Thyroid hormones (THs) play a major role regulating energy balance and brown adipose tissue (BAT) thermogenesis, as well as body temperature, as shown in hyperthyroid patients. However, the current landscape of preclinical thyroid hormone models is complex. For example, while rats become catabolic after TH administration, mice gain weight; so, these differences in species need to be analyzed in detail and specially whether temperature could be a factor. Here, we aimed to investigate the effect of environmental temperature on those actions. Rats were subcutaneously treated with L-thyroxine (T4) or stereotaxically within the ventromedial nucleus of the hypothalamus (VMH) with triiodothyronine (T3) and housed at 23°C, 4°C or 30°C; energy balance, BAT thermogenesis and AMP-activated protein kinase (AMPK) in the VMH were analyzed. Our data showed that the effect of both systemic T4 of central T3 on energy balance and BAT thermogenesis was dependent upon environmental temperature. This evidence is of interest in the design of experimental settings highlighting the species-specific metabolic actions of THs, and in understanding its physiological role in the adaptation to temperature.

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“… 28 , 29 It seems that BBSome is a critical determinant of the neuronal BMB-8B sensitivity. 30 The potential mechanism involving BBS1 gene in inducing obesity is supported by the loss of central BMP-8B response in mice carrying a single missense mutation in Bbs1 gene. 30 Other hypothesis of the development of obesity in BBS is that of impaired membrane expression of the leptin receptor (LepRB) in the hypothalamic cell population.…”

Section: Multidisciplinary Approachmentioning

confidence: 99%

“… 30 The potential mechanism involving BBS1 gene in inducing obesity is supported by the loss of central BMP-8B response in mice carrying a single missense mutation in Bbs1 gene. 30 Other hypothesis of the development of obesity in BBS is that of impaired membrane expression of the leptin receptor (LepRB) in the hypothalamic cell population. Leptin, a polypeptide hormone, binding to its receptor in the brain, decreases food intake and increases energy expenditure.…”

Section: Multidisciplinary Approachmentioning

confidence: 99%

Monitoring and Management of Bardet-Biedl Syndrome: What the Multi-Disciplinary Team Can Do

Caba¹,

Florea²,

Braha³

et al. 2022

JMDH

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Bardet -Biedl syndrome is a rare autosomal recessive multisystem non-motile ciliopathy. It has heterogeneous clinical manifestations. It is caused by mutations in 26 genes encoding BBSome proteins, chaperonines, and IFT complex. The main clinical features are: retinal cone-rod dystrophy, central obesity, postaxial polydactyly, cognitive impairment, hypogonadism and genitourinary anomalies, and kidney disease. The onset of clinical manifestations is variable which makes the diagnosis difficult in some patients. Because of the multiple system involvement, a multidisciplinary approach is necessary. The purpose of this review is to provide monitoring and management directions for a better approach to these patients.

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Obesity induces resistance to central action of BMP8B through a mechanism involving the BBSome

Cited by 7 publications

References 47 publications

Bardet‐Biedl syndrome: A focus on genetics, mechanisms and metabolic dysfunction

Bardet‐Biedl syndrome: A focus on genetics, mechanisms and metabolic dysfunction

Temperature modulates systemic and central actions of thyroid hormones on BAT thermogenesis

Monitoring and Management of Bardet-Biedl Syndrome: What the Multi-Disciplinary Team Can Do

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