Example of Molecular Metabolism format
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Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format
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Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format Example of Molecular Metabolism format
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open access Open Access

Molecular Metabolism — Template for authors

Publisher: Elsevier
Categories Rank Trend in last 3 yrs
Molecular Biology #44 of 382 up up by 6 ranks
Cell Biology #37 of 279 up up by 1 rank
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 643 Published Papers | 6895 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 09/06/2020
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Related Journals

open access Open Access
recommended Recommended

Taylor and Francis

Quality:  
High
CiteRatio: 15.1
SJR: 3.934
SNIP: 2.351
open access Open Access

Nature

Quality:  
High
CiteRatio: 6.7
SJR: 1.542
SNIP: 1.216
open access Open Access
recommended Recommended

American Association for the Advancement of Science

Quality:  
High
CiteRatio: 10.6
SJR: 3.659
SNIP: 1.504
open access Open Access
recommended Recommended

Springer

Quality:  
High
CiteRatio: 12.8
SJR: 2.928
SNIP: 1.815

Journal Performance & Insights

CiteRatio

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

A measure of average citations received per peer-reviewed paper published in the journal.

Measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

Measures actual citations received relative to citations expected for the journal's category.

10.7

8% from 2019

CiteRatio for Molecular Metabolism from 2016 - 2020
Year Value
2020 10.7
2019 9.9
2018 9.0
2017 10.0
2016 9.4
graph view Graph view
table view Table view

2.848

8% from 2019

SJR for Molecular Metabolism from 2016 - 2020
Year Value
2020 2.848
2019 3.107
2018 3.343
2017 3.997
2016 4.026
graph view Graph view
table view Table view

1.712

17% from 2019

SNIP for Molecular Metabolism from 2016 - 2020
Year Value
2020 1.712
2019 1.461
2018 1.467
2017 1.651
2016 1.517
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 8% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

insights Insights

  • SJR of this journal has decreased by 8% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 17% in last years.
  • This journal’s SNIP is in the top 10 percentile category.
Molecular Metabolism

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Elsevier

Molecular Metabolism

Molecular Metabolism is committed to serving as a platform reporting breakthroughs from all stages of the discovery and development of novel and improved personalized medicines for obesity, diabetes and associated diseases. The journal aims to publish hypothesis driven researc...... Read More

Molecular Biology

Cell Biology

Biochemistry, Genetics and Molecular Biology

i
Last updated on
09 Jun 2020
i
ISSN
2212-8778
i
Impact Factor
Maximum - 6.799
i
Acceptance Rate
Not provided
i
Frequency
Not provided
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
Green faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
elsarticle-num
i
Citation Type
Numbered
[25]
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Bibliography Example
G. E. Blonder, M. Tinkham, T. M. Klapwijk, Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion, Phys. Rev. B 25 (7) (1982) 4515–4532. URL 10.1103/PhysRevB.25.4515

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1016/J.MOLMET.2019.09.010
Glucagon-like peptide 1 (GLP-1)
30 Sep 2019 - Molecular metabolism

Abstract:

Background The glucagon-like peptide-1 (GLP-1) is a multifaceted hormone with broad pharmacological potential. Among the numerous metabolic effects of GLP-1 are the glucose-dependent stimulation of insulin secretion, decrease of gastric emptying, inhibition of food intake, increase of natriuresis and diuresis, and modulation ... Background The glucagon-like peptide-1 (GLP-1) is a multifaceted hormone with broad pharmacological potential. Among the numerous metabolic effects of GLP-1 are the glucose-dependent stimulation of insulin secretion, decrease of gastric emptying, inhibition of food intake, increase of natriuresis and diuresis, and modulation of rodent β-cell proliferation. GLP-1 also has cardio- and neuroprotective effects, decreases inflammation and apoptosis, and has implications for learning and memory, reward behavior, and palatability. Biochemically modified for enhanced potency and sustained action, GLP-1 receptor agonists are successfully in clinical use for the treatment of type-2 diabetes, and several GLP-1-based pharmacotherapies are in clinical evaluation for the treatment of obesity. Scope of review In this review, we provide a detailed overview on the multifaceted nature of GLP-1 and its pharmacology and discuss its therapeutic implications on various diseases. Major conclusions Since its discovery, GLP-1 has emerged as a pleiotropic hormone with a myriad of metabolic functions that go well beyond its classical identification as an incretin hormone. The numerous beneficial effects of GLP-1 render this hormone an interesting candidate for the development of pharmacotherapies to treat obesity, diabetes, and neurodegenerative disorders read more read less

Topics:

Gastric emptying (55%)55% related to the paper, Incretin (54%)54% related to the paper
View PDF
679 Citations
open accessOpen access Journal Article DOI: 10.1016/J.MOLMET.2014.02.002
Integrated physiology and systems biology of PPARα.
Sander Kersten1
01 Jul 2014 - Molecular metabolism

Abstract:

The Peroxisome Proliferator Activated Receptor alpha (PPARα) is a transcription factor that plays a major role in metabolic regulation. This review addresses the functional role of PPARα in intermediary metabolism and provides a detailed overview of metabolic genes targeted by PPARα, with a focus on liver. A distinction is ma... The Peroxisome Proliferator Activated Receptor alpha (PPARα) is a transcription factor that plays a major role in metabolic regulation. This review addresses the functional role of PPARα in intermediary metabolism and provides a detailed overview of metabolic genes targeted by PPARα, with a focus on liver. A distinction is made between the impact of PPARα on metabolism upon physiological, pharmacological, and nutritional activation. Low and high throughput gene expression analyses have allowed the creation of a comprehensive map illustrating the role of PPARα as master regulator of lipid metabolism via regulation of numerous genes. The map puts PPARα at the center of a regulatory hub impacting fatty acid uptake, fatty acid activation, intracellular fatty acid binding, mitochondrial and peroxisomal fatty acid oxidation, ketogenesis, triglyceride turnover, lipid droplet biology, gluconeogenesis, and bile synthesis/secretion. In addition, PPARα governs the expression of several secreted proteins that exert local and endocrine functions. read more read less

Topics:

Fatty acid binding (58%)58% related to the paper, Peroxisome proliferator-activated receptor alpha (56%)56% related to the paper, Lipid droplet (53%)53% related to the paper, Beta oxidation (52%)52% related to the paper, Lipid metabolism (52%)52% related to the paper
View PDF
447 Citations
open accessOpen access Journal Article DOI: 10.1016/J.MOLMET.2020.101102
GLP-1 receptor agonists in the treatment of type 2 diabetes - state-of-the-art.
Michael A. Nauck1, Daniel R. Quast1, Jakob Wefers1, Juris J. Meier1
01 Apr 2021 - Molecular metabolism

Abstract:

Background GLP-1 receptor agonists (GLP-1 RAs) with exenatide b.i.d. first approved to treat type 2 diabetes in 2005 have been further developed to yield effective compounds/preparations that have overcome the original problem of rapid elimination (short half-life), initially necessitating short intervals between injections (... Background GLP-1 receptor agonists (GLP-1 RAs) with exenatide b.i.d. first approved to treat type 2 diabetes in 2005 have been further developed to yield effective compounds/preparations that have overcome the original problem of rapid elimination (short half-life), initially necessitating short intervals between injections (twice daily for exenatide b.i.d.). Scope of review To summarize current knowledge about GLP-1 receptor agonist. Major conclusions At present, GLP-1 RAs are injected twice daily (exenatide b.i.d.), once daily (lixisenatide and liraglutide), or once weekly (exenatide once weekly, dulaglutide, albiglutide, and semaglutide). A daily oral preparation of semaglutide, which has demonstrated clinical effectiveness close to the once-weekly subcutaneous preparation, was recently approved. All GLP-1 RAs share common mechanisms of action: augmentation of hyperglycemia-induced insulin secretion, suppression of glucagon secretion at hyper- or euglycemia, deceleration of gastric emptying preventing large post-meal glycemic increments, and a reduction in calorie intake and body weight. Short-acting agents (exenatide b.i.d., lixisenatide) have reduced effectiveness on overnight and fasting plasma glucose, but maintain their effect on gastric emptying during long-term treatment. Long-acting GLP-1 RAs (liraglutide, once-weekly exenatide, dulaglutide, albiglutide, and semaglutide) have more profound effects on overnight and fasting plasma glucose and HbA1c, both on a background of oral glucose-lowering agents and in combination with basal insulin. Effects on gastric emptying decrease over time (tachyphylaxis). Given a similar, if not superior, effectiveness for HbA1c reduction with additional weight reduction and no intrinsic risk of hypoglycemic episodes, GLP-1RAs are recommended as the preferred first injectable glucose-lowering therapy for type 2 diabetes, even before insulin treatment. However, GLP-1 RAs can be combined with (basal) insulin in either free- or fixed-dose preparations. More recently developed agents, in particular semaglutide, are characterized by greater efficacy with respect to lowering plasma glucose as well as body weight. Since 2016, several cardiovascular (CV) outcome studies have shown that GLP-1 RAs can effectively prevent CV events such as acute myocardial infarction or stroke and associated mortality. Therefore, guidelines particularly recommend treatment with GLP-1 RAs in patients with pre-existing atherosclerotic vascular disease (for example, previous CV events). The evidence of similar effects in lower-risk subjects is not quite as strong. Since sodium/glucose cotransporter-2 (SGLT-2) inhibitor treatment reduces CV events as well (with the effect mainly driven by a reduction in heart failure complications), the individual risk of ischemic or heart failure complications should guide the choice of treatment. GLP-1 RAs may also help prevent renal complications of type 2 diabetes. Other active research areas in the field of GLP-1 RAs are the definition of subgroups within the type 2 diabetes population who particularly benefit from treatment with GLP-1 RAs. These include pharmacogenomic approaches and the characterization of non-responders. Novel indications for GLP-1 RAs outside type 2 diabetes, such as type 1 diabetes, neurodegenerative diseases, and psoriasis, are being explored. Thus, within 15 years of their initial introduction, GLP-1 RAs have become a well-established class of glucose-lowering agents that has the potential for further development and growing impact for treating type 2 diabetes and potentially other diseases. read more read less

Topics:

Semaglutide (66%)66% related to the paper, Exenatide (61%)61% related to the paper, Albiglutide (60%)60% related to the paper, Liraglutide (59%)59% related to the paper, Dulaglutide (58%)58% related to the paper
361 Citations
open accessOpen access Journal Article DOI: 10.1016/J.MOLMET.2018.09.009
LY3298176, a novel dual GIP and GLP-1 receptor agonist for the treatment of type 2 diabetes mellitus: From discovery to clinical proof of concept.
03 Oct 2018 - Molecular metabolism

Abstract:

Objective A novel dual GIP and GLP-1 receptor agonist, LY3298176, was developed to determine whether the metabolic action of GIP adds to the established clinical benefits of selective GLP-1 receptor agonists in type 2 diabetes mellitus (T2DM). Methods LY3298176 is a fatty acid modified peptide with dual GIP and GLP-1 receptor... Objective A novel dual GIP and GLP-1 receptor agonist, LY3298176, was developed to determine whether the metabolic action of GIP adds to the established clinical benefits of selective GLP-1 receptor agonists in type 2 diabetes mellitus (T2DM). Methods LY3298176 is a fatty acid modified peptide with dual GIP and GLP-1 receptor agonist activity designed for once-weekly subcutaneous administration. LY3298176 was characterised in vitro, using signaling and functional assays in cell lines expressing recombinant or endogenous incretin receptors, and in vivo using body weight, food intake, insulin secretion and glycemic profiles in mice. A Phase 1, randomised, placebo-controlled, double-blind study was comprised of three parts: a single-ascending dose (SAD; doses 0.25–8 mg) and 4-week multiple-ascending dose (MAD; doses 0.5–10 mg) studies in healthy subjects (HS), followed by a 4-week multiple-dose Phase 1 b proof-of-concept (POC; doses 0.5–15 mg) in patients with T2DM ( ClinicalTrials.gov no. NCT02759107). Doses higher than 5 mg were attained by titration, dulaglutide (DU) was used as a positive control. The primary objective was to investigate safety and tolerability of LY3298176. Results LY3298176 activated both GIP and GLP-1 receptor signaling in vitro and showed glucose-dependent insulin secretion and improved glucose tolerance by acting on both GIP and GLP-1 receptors in mice. With chronic administration to mice, LY3298176 potently decreased body weight and food intake; these effects were significantly greater than the effects of a GLP-1 receptor agonist. A total of 142 human subjects received at least 1 dose of LY3298176, dulaglutide, or placebo. The PK profile of LY3298176 was investigated over a wide dose range (0.25–15 mg) and supports once-weekly administration. In the Phase 1 b trial of diabetic subjects, LY3298176 doses of 10 mg and 15 mg significantly reduced fasting serum glucose compared to placebo (least square mean [LSM] difference [95% CI]: −49.12 mg/dL [−78.14, −20.12] and −43.15 mg/dL [−73.06, −13.21], respectively). Reductions in body weight were significantly greater with the LY3298176 1.5 mg, 4.5 mg and 10 mg doses versus placebo in MAD HS (LSM difference [95% CI]: −1.75 kg [−3.38, −0.12], −5.09 kg [−6.72, −3.46] and −4.61 kg [−6.21, −3.01], respectively) and doses of 10 mg and 15 mg had a relevant effect in T2DM patients (LSM difference [95% CI]: −2.62 kg [−3.79, −1.45] and −2.07 kg [−3.25, −0.88], respectively. The most frequent side effects reported with LY3298176 were gastrointestinal (vomiting, nausea, decreased appetite, diarrhoea, and abdominal distension) in both HS and patients with T2DM; all were dose-dependent and considered mild to moderate in severity. Conclusions Based on these results, the pharmacology of LY3298176 translates from preclinical to clinical studies. LY3298176 has the potential to deliver clinically meaningful improvement in glycaemic control and body weight. The data warrant further clinical evaluation of LY3298176 for the treatment of T2DM and potentially obesity. read more read less

Topics:

Receptor agonist activity (62%)62% related to the paper, Dulaglutide (57%)57% related to the paper, Incretin (56%)56% related to the paper, Agonist (55%)55% related to the paper, Glucagon-like peptide 1 receptor (55%)55% related to the paper
339 Citations
open accessOpen access Journal Article DOI: 10.1016/J.MOLMET.2017.06.019
Human beta cell mass and function in diabetes: Recent advances in knowledge and technologies to understand disease pathogenesis
Chunguang Chen1, Christian M. Cohrs1, Julia Stertmann1, Robert Bozsak1, Stephan Speier1
01 Sep 2017 - Molecular metabolism

Abstract:

Background Plasma insulin levels are predominantly the product of the morphological mass of insulin producing beta cells in the pancreatic islets of Langerhans and the functional status of each of these beta cells. Thus, deficiency in either beta cell mass or function, or both, can lead to insufficient levels of insulin, res... Background Plasma insulin levels are predominantly the product of the morphological mass of insulin producing beta cells in the pancreatic islets of Langerhans and the functional status of each of these beta cells. Thus, deficiency in either beta cell mass or function, or both, can lead to insufficient levels of insulin, resulting in hyperglycemia and diabetes. Nonetheless, the precise contribution of beta cell mass and function to the pathogenesis of diabetes as well as the underlying mechanisms are still unclear. In the past, this was largely due to the restricted number of technologies suitable for studying the scarcely accessible human beta cells. However, in recent years, a number of new platforms have been established to expand the available techniques and to facilitate deeper insight into the role of human beta cell mass and function as cause for diabetes and as potential treatment targets. read more read less

Topics:

Beta cell (58%)58% related to the paper, Pancreatic islets (55%)55% related to the paper
333 Citations
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Absolutely not! Our tool has been designed to help you focus on writing. You can write your entire paper as per the Molecular Metabolism guidelines and auto format it.

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Yes, the template is compliant with the Molecular Metabolism guidelines. Our experts at SciSpace ensure that. If there are any changes to the journal's guidelines, we'll change our algorithm accordingly.

3. Can I cite my article in multiple styles in Molecular Metabolism?

Of course! We support all the top citation styles, such as APA style, MLA style, Vancouver style, Harvard style, and Chicago style. For example, when you write your paper and hit autoformat, our system will automatically update your article as per the Molecular Metabolism citation style.

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Sign up for our free trial, and you'll be able to use all our features for seven days. You'll see how helpful they are and how inexpensive they are compared to other options, Especially for Molecular Metabolism.

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12. Is Molecular Metabolism's impact factor high enough that I should try publishing my article there?

To be honest, the answer is no. The impact factor is one of the many elements that determine the quality of a journal. Few of these factors include review board, rejection rates, frequency of inclusion in indexes, and Eigenfactor. You need to assess all these factors before you make your final call.

13. What is Sherpa RoMEO Archiving Policy for Molecular Metabolism?

SHERPA/RoMEO Database

We extracted this data from Sherpa Romeo to help researchers understand the access level of this journal in accordance with the Sherpa Romeo Archiving Policy for Molecular Metabolism. The table below indicates the level of access a journal has as per Sherpa Romeo's archiving policy.

RoMEO Colour Archiving policy
Green Can archive pre-print and post-print or publisher's version/PDF
Blue Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow Can archive pre-print (ie pre-refereeing)
White Archiving not formally supported
FYI:
  1. Pre-prints as being the version of the paper before peer review and
  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

14. What are the most common citation types In Molecular Metabolism?

The 5 most common citation types in order of usage for Molecular Metabolism are:.

S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
5. Footnote

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Yes, SciSpace provides this functionality. After signing up, you would need to import your existing references from Word or Bib file to SciSpace. Then SciSpace would allow you to download your references in Molecular Metabolism Endnote style according to Elsevier guidelines.

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