首页> 外文期刊>Clinical lipidology. >Depot- and obesity-related differences in adipogenesisAdipocyte hypertrophy and hyperplasia are known to facilitate lipid storage in adipose tissues by increasing adipocyte cell size and number, respectively. Adipogenesis is the process resulting in adipose tissue hyperplasia. Although depot-specific differences and obesity-related modulation of adipocyte size are well documented, available data on adipogenesis and adipose tissue hyperplasia are less conclusive. Most studies support a reduction of adipogenesis in the obese state. Preadipocytes of the subcutaneous fat depot appear to be more responsive to adipogenic stimulation compared with those from visceral fat compartments in most studies. A number of studies support the notion that adipose tissue expansion through hyperplasia reduces ectopic lipid excess and obesity-related complications. Several genetic variants have been identified in the genes coding for adipogenesis-regulating proteins. While some of these variants have been clearly associated with the phenotypes of obesity and obesity-related alterations, available data highlight the importance of considering gene–gene and gene–diet interactions.
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Depot- and obesity-related differences in adipogenesisAdipocyte hypertrophy and hyperplasia are known to facilitate lipid storage in adipose tissues by increasing adipocyte cell size and number, respectively. Adipogenesis is the process resulting in adipose tissue hyperplasia. Although depot-specific differences and obesity-related modulation of adipocyte size are well documented, available data on adipogenesis and adipose tissue hyperplasia are less conclusive. Most studies support a reduction of adipogenesis in the obese state. Preadipocytes of the subcutaneous fat depot appear to be more responsive to adipogenic stimulation compared with those from visceral fat compartments in most studies. A number of studies support the notion that adipose tissue expansion through hyperplasia reduces ectopic lipid excess and obesity-related complications. Several genetic variants have been identified in the genes coding for adipogenesis-regulating proteins. While some of these variants have been clearly associated with the phenotypes of obesity and obesity-related alterations, available data highlight the importance of considering gene–gene and gene–diet interactions.

机译:脂肪形成与肥胖相关的差异已知脂肪细胞肥大和增生分别通过增加脂肪细胞的大小和数量来促进脂质在脂肪组织中的存储。脂肪形成是导致脂肪组织增生的过程。尽管已经有很多文献记载了贮库特异性差异和肥胖相关的脂肪细胞大小调节,但有关脂肪形成和脂肪组织增生的可用数据尚无定论。大多数研究支持在肥胖状态下减少脂肪形成。在大多数研究中,与来自内脏脂肪区室的脂肪细胞相比,皮下脂肪库的前脂肪细胞似乎对脂肪刺激更为敏感。许多研究支持这样的观点,即通过增生的脂肪组织扩张可以减少异位脂质过多和肥胖相关的并发症。在编码脂肪形成调节蛋白的基因中已经鉴定出几种遗传变异。尽管其中一些变异与肥胖症的表型和与肥胖有关的改变明显相关,但现有数据突出了考虑基因-基因和基因-饮食相互作用的重要性。

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Adipocyte hypertrophy and hyperplasia are known to facilitate lipid storage in adipose tissues by increasing adipocyte cell size and number, respectively. Adipogenesis is the process resulting in adipose tissue hyperplasia.Although depot-specific differences and obesity-related modulation of adipocyte size are well documented,available data on adipogenesis and adipose tissue hyperplasia are less conclusive. Most studies support a reduction of adipogenesis in the obese state. Preadipocytes of the subcutaneous fat depot appear to be more responsive to adipogenic stimulation compared with those from visceral fat compartments in most studies. A number of studies support the notion that adipose tissue expansion through hyperplasia reduces ectopic lipid excess and obesity-related complications. Several genetic variants have been identified in the genes coding for adipogenesis-regulating proteins. While some of these variants have been clearly associated with the phenotypes of obesity and obesity-related alterations, available data highlight the importance of considering gene–gene and gene–diet interactions.
机译:已知脂肪细胞肥大和增生分别通过增加脂肪细胞的大小和数量来促进脂质在脂肪组织中的储存。脂肪生成是导致脂肪组织增生的过程。尽管已经有很多文献记载了贮库特异性差异和肥胖相关的脂肪细胞大小调节,但有关脂肪生成和脂肪组织增生的可用数据尚无定论。大多数研究支持在肥胖状态下减少脂肪形成。在大多数研究中,与来自内脏脂肪区室的脂肪细胞相比,皮下脂肪库的前脂肪细胞似乎对脂肪刺激更为敏感。许多研究支持这样的观点,即通过增生的脂肪组织扩张可以减少异位脂质过多和肥胖相关的并发症。在编码脂肪形成调节蛋白的基因中已经鉴定出几种遗传变异。尽管其中一些变异与肥胖症的表型和与肥胖有关的改变明显相关,但现有数据突出了考虑基因-基因和基因-饮食相互作用的重要性。

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