Scd1 is expressed in sebaceous glands and is disrupted in the asebia mouse

Zheng, Ying; Eilertsen, Kenneth J.; Ge, Lan; Zhang, Lin; Sundberg, John P.; Prouty, Stephen M.; Stenn, Kurt S.; Parimoo, Satish

doi:10.1038/15446

Cited by 219 publications

(187 citation statements)

References 14 publications

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“…In adult mice, Scd1 is found in presebocytes and Scd3 in mature sebocytes [6]. Mice with a targeted deletion of Scd1 or naturally occurring asebia mutation have hypoplasia of the sebaceous and meibomian glands resulting in alopecia and closed eye fissure [2,41,68]. The hypoplasia of sebaceous glands in adult scd1-deficient mice results in loss of Scd3 expression in the skin [6].…”

Section: Importance Of Scd For Skin Biology and Developmentmentioning

confidence: 99%

“…The skin expresses three isoforms of SCD, Scd1-Scd3 [6,12,41]. In adult mice, Scd1 is found in presebocytes and Scd3 in mature sebocytes [6].…”

Section: Importance Of Scd For Skin Biology and Developmentmentioning

confidence: 99%

“…Mice with a targeted deletion of Scd1 or with spontaneous asebia mutations in Scd1 have provided several novel insights into the metabolic role of SCD1 [2,41]. scd1-deficient mice have reduced fatty acid and triglyceride synthesis in response to high-carbohydrate feeding [1,4,22].…”

Section: The Effect Of Scd1 Deficiency On Lipid Synthesis and Oxidationmentioning

confidence: 99%

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Role of stearoyl-coenzyme A desaturase in regulating lipid metabolism

Flowers

Ntambi

2008

Current Opinion in Lipidology

374

312

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Purpose of review-Stearoyl-coenzyme A desaturase 1 is a δ-9 fatty acid desaturase that catalyzes the synthesis of monounsaturated fatty acids and has emerged as a key regulator of metabolism. This review evaluates the latest advances in our understanding of the pivotal role of stearoyl-coenzyme A desaturase 1 in health and disease.Recent findings-scd1-deficient mice have reduced lipid synthesis and enhanced lipid oxidation, thermogenesis and insulin sensitivity in various tissues including liver, muscle and adipose tissue due to transcriptional and posttranscriptional effects. These metabolic changes protect scd1-deficient mice from a variety of dietary, pharmacological and genetic conditions that promote obesity, insulin resistance and hepatic steatosis. Stearoylcoenzyme A desaturase 1 is required to guard against dietary unsaturated fat deficiency, leptin deficiency-induced diabetes, and palmitate-induced lipotoxic insults in muscle and pancreatic β-cells. Paradoxical observations of increased muscle stearoyl-coenzyme A desaturase 1 during obesity, starvation and exercise raise questions as to the role of stearoyl-coenzyme A desaturase 1 in this tissue. Mice with a liverspecific loss of stearoyl-coenzyme A desaturase 1, and inhibition of stearoyl-coenzyme A desaturase 1 via antisense or RNA interference, recapitulate only a subset of the phenotypes observed in global Scd1 deficiency, indicating the involvement of multiple tissues.Summary-Recent studies in humans and animal models have highlighted that modulation of stearoyl-coenzyme A desaturase 1 activity by dietary intervention or genetic manipulation strongly influences several facets of energy metabolism to affect susceptibility to obesity, insulin resistance, diabetes and hyperlipidemia.

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Section: Importance Of Scd For Skin Biology and Developmentmentioning

confidence: 99%

“…The skin expresses three isoforms of SCD, Scd1-Scd3 [6,12,41]. In adult mice, Scd1 is found in presebocytes and Scd3 in mature sebocytes [6].…”

Section: Importance Of Scd For Skin Biology and Developmentmentioning

confidence: 99%

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Role of stearoyl-coenzyme A desaturase in regulating lipid metabolism

Flowers

Ntambi

2008

Current Opinion in Lipidology

374

312

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“…New insights into the physiological role of the SCD1 gene and its endogenous products came from recent studies of the asebia mouse strains (ab j and ab 2j ) that have naturally occurring mutations in SCD1 (17)(18)(19) as well as a laboratory mouse model with a targeted disruption (SCD1Ϫ͞Ϫ) (6). We used these animal models to show that SCD1Ϫ͞Ϫ mice are deficient in hepatic triglycerides and cholesterol esters (7,20).…”

mentioning

confidence: 99%

“…The existence of multiple SCD isoforms in mice (6,(14)(15)(16)(17)(18) and rats makes it difficult to determine the role of each isoform in lipid metabolism. New insights into the physiological role of the SCD1 gene and its endogenous products came from recent studies of the asebia mouse strains (ab j and ab 2j ) that have naturally occurring mutations in SCD1 (17)(18)(19) as well as a laboratory mouse model with a targeted disruption (SCD1Ϫ͞Ϫ) (6).…”

mentioning

confidence: 99%

Loss of stearoyl–CoA desaturase-1 function protects mice against adiposity

Ntambi

Miyazaki

Stoehr

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

983

913

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Stearoyl-CoA desaturase (SCD) is a central lipogenic enzyme catalyzing the synthesis of monounsaturated fatty acids, mainly oleate (C18:1) and palmitoleate (C16:1), which are components of membrane phospholipids, triglycerides, wax esters, and cholesterol esters. Several SCD isoforms (SCD1-3) exist in the mouse. Here we show that mice with a targeted disruption of the SCD1 isoform have reduced body adiposity, increased insulin sensitivity, and are resistant to diet-induced weight gain. The protection from obesity involves increased energy expenditure and increased oxygen consumption. Compared with the wild-type mice the SCD1؊͞؊ mice have increased levels of plasma ketone bodies but reduced levels of plasma insulin and leptin. In the SCD1؊͞؊ mice, the expression of several genes of lipid oxidation are up-regulated, whereas lipid synthesis genes are down-regulated. These observations suggest that a consequence of SCD1 deficiency is an activation of lipid oxidation in addition to reduced triglyceride synthesis and storage.S tearoyl-CoA desaturase (SCD) is the rate-limiting enzyme in the biosynthesis of monounsaturated fatty acids. It catalyzes the introduction of the cis double bond in the ⌬9 position of fatty acyl-CoA substrates. The preferred desaturation substrates are palmitoyl-CoA and stearoyl-CoA, which are converted to palmitoleoyl-CoA (16:1) and oleoyl-CoA (18:1), respectively (1-4). These fatty acids are requisite components of membrane phospholipids, triglycerides, cholesterol esters, and wax esters (5-7). Effects on composition of phospholipids ultimately determine membrane fluidity, and the effects on the composition of cholesterol esters and triglycerides can affect lipoprotein metabolism and adiposity. SCD expression is sensitive to dietary factors including polyunsaturated fatty acids, cholesterol and vitamin A, hormonal changes (i.e., insulin and glucagon), developmental processes, temperature changes, thiazolinediones, metals, alcohol, peroxisomal proliferators, and phenolic compounds (3). High SCD activity has been implicated in a wide range of disorders including diabetes, atherosclerosis, cancer, obesity, and viral infection (3,(8)(9)(10)(11)(12)(13).The existence of multiple SCD isoforms in mice (6, 14-18) and rats makes it difficult to determine the role of each isoform in lipid metabolism. New insights into the physiological role of the SCD1 gene and its endogenous products came from recent studies of the asebia mouse strains (ab j and ab 2j ) that have naturally occurring mutations in SCD1 (17-19) as well as a laboratory mouse model with a targeted disruption (SCD1Ϫ͞Ϫ) (6). We used these animal models to show that SCD1Ϫ͞Ϫ mice are deficient in hepatic triglycerides and cholesterol esters (7,20). The levels of palmitoleate (16:1) and oleate (18:1) are reduced, whereas palmitate and stearate are increased in the lipid fractions of SCD1Ϫ͞Ϫ mice. On a high carbohydrate diet supplemented with triolein, the cholesterol ester levels are corrected but the triglyceride levels are not reversed to the ...

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