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Emerging regulation and function of betatrophin.

ABSTRACT: Betatrophin, also known as TD26/RIFL/lipasin/ANGPTL8/C19orf80, is a novel protein predominantly expressed in human liver. To date, several betatrophin orthologs have been identified in mammals. Increasing evidence has revealed an association between betatrophin expression and serum lipid profiles, particularly in patients with obesity or diabetes. Stimulators of betatrophin, such as insulin, thyroid hormone, irisin and caloric intake, are usually relevant to energy expenditure or thermogenesis. In murine models, serum triglyceride levels as well as pancreatic cell proliferation are potently enhanced by betatrophin. Intriguingly, conflicting phenomena have also been reported that betatrophin suppresses hepatic triglyceride levels, suggesting that betatrophin function is mediated by complex regulatory processes. However, its precise physiological role remains unclear at present. In this review, we have summarized the current findings on betatrophin and their implications.

SUBMITTER: Tseng YH

PROVIDER: S-EPMC4284785 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Emerging regulation and function of betatrophin.

Tseng Yi-Hsin YH Yeh Yung-Hsin YH Chen Wei-Jan WJ Lin Kwang-Huei KH

International journal of molecular sciences 20141218 12

Betatrophin, also known as TD26/RIFL/lipasin/ANGPTL8/C19orf80, is a novel protein predominantly expressed in human liver. To date, several betatrophin orthologs have been identified in mammals. Increasing evidence has revealed an association between betatrophin expression and serum lipid profiles, particularly in patients with obesity or diabetes. Stimulators of betatrophin, such as insulin, thyroid hormone, irisin and caloric intake, are usually relevant to energy expenditure or thermogenesis. ...[more]

PMID: 25530616

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Betatrophin.

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| S-EPMC4594198 | biostudies-literature

Emerging Insights into the Function of Kinesin-8 Proteins in Microtubule Length Regulation.

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Plasma Betatrophin Levels and Carotid Atherosclerosis.

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Cloning, expression, and spectral analysis of mouse betatrophin.

Project description:Background: Betatrophin, a novel secretory protein from liver and fatty tissues, is believed to be involved in lipid and glucose metabolism. However, its precise physiological role remains unclear. Here, we report the cloning, expression, and purification steps of mouse betatrophin in a prokaryotic system, followed by its structural analysis. Methods: Specific cloning primers were used to amplify the coding sequence of mouse liver betatrophin. The product was cloned into pET28 and expressed in E.coli BL21 (DE3) cells. The suitability of the refolding procedure was assessed by determining secondary structures of the initial and refolded proteins using circular dichroism spectroscopy. Results: The polymerase chain reaction resulted in a 549 bp nucleotide sequence, encoding a 183 amino acid polypeptide, with an apparent molecular weight of 21 kDa, which was expressed in an inclusion body. Following an optimization and refolding procedure, the recombinant protein was purified by anion exchange and metal affinity chromatography. CD spectra revealed that the refolded protein has suitable configuration. Conclusion: We believe that the produced betatrophin is suitable for further biochemical studies on glucose and lipid metabolism.

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ANGPTL8/betatrophin does not control pancreatic beta cell expansion.

Project description:Recently, it was reported that angiopoietin-like protein 8 (ANGPTL8) was the long-sought "betatrophin" that could control pancreatic beta cell proliferation. However, studies of Angptl8(?/?) mice revealed profound reduction of triglyceride levels, but no abnormalities in glucose homeostasis. We now report that Angptl8(?/?) mice undergo entirely normal beta cell expansion in response to insulin resistance resulting from either a high-fat diet or from the administration of the insulin receptor antagonist S961. Furthermore, overexpression of ANGPTL8 in livers of mice doubles plasma triglyceride levels, but does not alter beta cell expansion nor glucose metabolism. These data indicate that ANGPTL8 does not play a role in controlling beta cell growth, nor can it be given to induce such expansion. The findings that plasma triglyceride levels are reduced by Angptl8 deletion and increased following ANGPTL8 overexpression support the possibility that inhibition of ANGPTL8 represents a therapeutic strategy for hypertriglyceridemia.

| S-EPMC4243040 | biostudies-literature

Cloning, Expression, Purification and CD Analysis of Recombinant Human Betatrophin.

Project description:Background:Betatrophin is a member of the angiopoietin-like (ANGPTL) family that has been implicated in both triglyceride and glucose metabolism. The physiological functions and molecular targets of this protein remain largely unknown; hence, a purified available protein would aid study of the exact role of betatrophin in lipid or glucose metabolism. Methods:In this study, we cloned the full-length cDNA of betatrophin from a human liver cDNA library. Betatrophin was expressed in the pET-21b-E. coli Bl21 (DE3) system and purified by immobilized metal-affinity chromatography and ion-exchange chromatography. Results:Circular dichroism spectroscopy revealed ?-helix as the major regular secondary structure in recombinant betatrophin. Conclusion:The production method is based on commonly available resources; therefore, it can be readily implemented.

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Circulating Betatrophin in Patients with Type 2 Diabetes: A Meta-Analysis.

Project description:ObjectiveTo investigate the association between circulating betatrophin level and type 2 diabetes mellitus (T2DM) in human.MethodsA comprehensive literature search was performed in PubMed and Embase databases to identify eligible studies assessing the circulating levels of betatrophin in both T2DM patients and nondiabetic adults.ResultsA total of nine eligible studies with twelve comparisons were included for the final meta-analysis. Circulating betatrophin levels in T2DM patients were higher than those in the nondiabetic controls (random-effect SMD 0.53; 95% CI 0.13 to 0.94; P = 0.010). In the subgroup of nonobese population but not the obese population, the overall betatrophin level in T2DM patients was much higher than that in the nondiabetic controls (nonobese: random-effect SMD, 0.82; 95% CI 0.42 to 1.21; P < 0.001; obese: random-effect SMD, -0.39; 95% CI, -0.95 to 0.18; P = 0.18). Metaregression indicated that body mass index of T2DM patients was associated with mean difference of betatrophin level between T2DM and nondiabetic adults (slope, -578.8; t = -2.7; P = 0.02).ConclusionBased on the findings of our meta-analysis, circulating betatrophin level of T2DM patients is higher than that of nondiabetic adults in the nonobese population, but not in the obese population.

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