Cited by 143Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismLipid metabolism and biosynthesis

The DOI matches its Crossref record; 264 of the 264 references it cites were found in a registry or an index.

Adipose tissue hyperplasia and hypertrophy in common and syndromic obesity-the case of BBS obesity

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Horwitz, Avital, Birk, Ruth·2023·Nutrients

Abstract

Obesity is a metabolic state generated by the expansion of adipose tissue. Adipose tissue expansion depends on the interplay between hyperplasia and hypertrophy, and is mainly regulated by a complex interaction between genetics and excess energy intake. However, the genetic regulation of adipose tissue expansion is yet to be fully understood. Obesity can be divided into common multifactorial/polygenic obesity and monogenic obesity, non-syndromic and syndromic. Several genes related to obesity were found through studies of monogenic non-syndromic obesity models. However, syndromic obesity, characterized by additional features other than obesity, suggesting a more global role of the mutant genes related to the syndrome and, thus, an additional peripheral influence on the development of obesity, were hardly studied to date in this regard. This review summarizes present knowledge regarding the hyperplasia and hypertrophy of adipocytes in common obesity. Additionally, we highlight the scarce research on syndromic obesity as a model for studying adipocyte hyperplasia and hypertrophy, focusing on Bardet–Biedl syndrome (BBS). BBS obesity involves central and peripheral mechanisms, with molecular and mechanistic alternation in adipocyte hyperplasia and hypertrophy. Thus, we argue that using syndromic obesity models, such as BBS, can further advance our knowledge regarding peripheral adipocyte regulation in obesity.

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Crossref · 10.3390/nu15153445

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Scheme 1 Hyperplasia and hypertrophy in adipose tissue. Pluripotent MSC commit to differentiate into APC lineage located in the stromovascular fraction of adipose tissue, and APCs differentiate into mature adipocyte. Adipose tissue expands by increasing the volume of pre-existing adipocytes (adipose hypertrophy), and by generating new small adipocytes (hyperplasia). Increased adipocyte size correlates with impaired adipose tissue function, increased local inflammation, and decreased lipid storage capacity. ↑ increase, ↓ decrease, ↔ no change. Adapted from “Metabolically Unhealthy Obesity” and “Metabolically Healthy Obesity” by BioRender.com (2022). Retrieved from https://app.biorender.com/biorender-templates (accessed on 16 July 2023).
Scheme 1 Hyperplasia and hypertrophy in adipose tissue. Pluripotent MSC commit to differentiate into APC lineage located in the stromovascular fraction of adipose tissue, and APCs differentiate into mature adipocyte. Adipose tissue expands by increasing the volume of pre-existing adipocytes (adipose hypertrophy), and by generating new small adipocytes (hyperplasia). Increased adipocyte size correlates with impaired adipose tissue function, increased local inflammation, and decreased lipid storage capacity. ↑ increase, ↓ decrease, ↔ no change. Adapted from “Metabolically Unhealthy Obesity” and “Metabolically Healthy Obesity” by BioRender.com (2022). Retrieved from https://app.biorender.com/biorender-templates (accessed on 16 July 2023).CC BY · PubMed Central
Scheme 2 The leptin–melanocortin signaling pathways: Leptin, secreted from adipose tissue, activates leptin receptors on POMC expressing neurons in the arcuate nucleus, leading to the secretion of α-MSH. α-MSH is an agonist of the MC4R expressed in the paraventricular nucleus, up-regulating the conversion of ATP to cAMP and regulating satiety and energy expenditure. Setmelanotide is an α-MSH analog and a pharmacological agonist of MC4R, activating the melanocortin signaling cascade. The scheme was created with BioRender.com.
Scheme 2 The leptin–melanocortin signaling pathways: Leptin, secreted from adipose tissue, activates leptin receptors on POMC expressing neurons in the arcuate nucleus, leading to the secretion of α-MSH. α-MSH is an agonist of the MC4R expressed in the paraventricular nucleus, up-regulating the conversion of ATP to cAMP and regulating satiety and energy expenditure. Setmelanotide is an α-MSH analog and a pharmacological agonist of MC4R, activating the melanocortin signaling cascade. The scheme was created with BioRender.com.CC BY · PubMed Central
Scheme 3 The genetics of obesity. Hyperplasia and hypertrophy of adipose tissue leads to adipose tissue expansion and obesity development. Obesity can be divided broadly into two categories: Common polygenic obesity and genetic obesity. The scheme was created with BioRender.com.
Scheme 3 The genetics of obesity. Hyperplasia and hypertrophy of adipose tissue leads to adipose tissue expansion and obesity development. Obesity can be divided broadly into two categories: Common polygenic obesity and genetic obesity. The scheme was created with BioRender.com.CC BY · PubMed Central

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  1. Macdougald, O.A. (2014). Methods in Enzymology, Academic Press. [1st ed.].

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Authors
Horwitz, A., & Birk, R.
Affiliations
Ariel University (IL)
Corresponding author
Birk, Ruth
Venue
Nutrients
Publisher
MDPI AG
Published
2023-08-04
Volume
15
Issue
15
Pages
3445
ISSN
2072-6643 (ISSN-L)
OpenAlex
W4385577907
Cited by
143
References
264
Citations by year
2026: 50 · 2025: 52 · 2024: 37 · 2023: 4
FWCI
5.59
Type
journal article
Language
en
Open access
Locations
  • Nutrients (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords
adipose tissue hyperplasia, adipocyte hypertrophy, syndromic obesity, Bardet-Biedl syndrome, monogenic obesity, polygenic obesity
MeSH terms
Adipose Tissue, Animals, Humans, Hyperplasia, Hypertrophy, Obesity, Syndrome, Adipocytes, Bardet-Biedl Syndrome

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