Example of Current Diabetes Reviews format
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Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format
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Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format Example of Current Diabetes Reviews format
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This content is only for preview purposes. The original open access content can be found here.
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Current Diabetes Reviews — Template for authors

Publisher: Bentham Science
Categories Rank Trend in last 3 yrs
Endocrinology, Diabetes and Metabolism #117 of 219 down down by 28 ranks
Endocrinology #77 of 117 down down by 14 ranks
journal-quality-icon Journal quality:
Medium
calendar-icon Last 4 years overview: 277 Published Papers | 960 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 08/07/2020
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Top papers
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FAQ

Related Journals

open access Open Access

Springer

Quality:  
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CiteRatio: 6.0
SJR: 1.141
SNIP: 1.158
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open access Open Access

Springer

Quality:  
High
CiteRatio: 6.1
SJR: 1.034
SNIP: 1.318

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.

3.5

13% from 2019

CiteRatio for Current Diabetes Reviews from 2016 - 2020
Year Value
2020 3.5
2019 4.0
2018 3.6
2017 4.2
2016 5.1
graph view Graph view
table view Table view

0.631

8% from 2019

SJR for Current Diabetes Reviews from 2016 - 2020
Year Value
2020 0.631
2019 0.687
2018 0.733
2017 0.879
2016 1.396
graph view Graph view
table view Table view

1.065

1% from 2019

SNIP for Current Diabetes Reviews from 2016 - 2020
Year Value
2020 1.065
2019 1.052
2018 0.842
2017 0.996
2016 1.213
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has decreased by 13% 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 1% in last years.
  • This journal’s SNIP is in the top 10 percentile category.
Current Diabetes Reviews

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Bentham Science

Current Diabetes Reviews

Current Diabetes Reviews publishes frontier reviews, drug clinical trial studies and guest edited issues on all the latest advances on diabetes and its related areas dedicated to clinical research e.g. pharmacology, pathogenesis, complications, epidemiology, clinical care and ...... Read More

Endocrinology, Diabetes and Metabolism

Medicine

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Last updated on
08 Jul 2020
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ISSN
1573-3998
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Impact Factor
High - 1.065
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Open Access
No
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Sherpa RoMEO Archiving Policy
Yellow faq
i
Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Bibliography Name
Vancouver
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Citation Type
Numbered
[25]
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Bibliography Example
Blonder, G E, Tinkham, M, & Klapwijk, T M. Transition from metallic to tunnel- ing regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B. 2013;87(10):100510.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.2174/157339913804143225
Regulation of insulin synthesis and secretion and pancreatic Beta-cell dysfunction in diabetes
Zhuo Fu1, Elizabeth R. Gilbert, Dongmin Liu
31 Dec 2012 - Current Diabetes Reviews

Abstract:

Pancreatic β-cell dysfunction plays an important role in the pathogenesis of both type 1 and type 2 diabetes. Insulin, which is produced in β-cells, is a critical regulator of metabolism. Insulin is synthesized as preproinsulin and processed to proinsulin. Proinsulin is then converted to insulin and C-peptide and stored in se... Pancreatic β-cell dysfunction plays an important role in the pathogenesis of both type 1 and type 2 diabetes. Insulin, which is produced in β-cells, is a critical regulator of metabolism. Insulin is synthesized as preproinsulin and processed to proinsulin. Proinsulin is then converted to insulin and C-peptide and stored in secretary granules awaiting release on demand. Insulin synthesis is regulated at both the transcriptional and translational level. The cis-acting sequences within the 5' flanking region and trans-activators including paired box gene 6 (PAX6), pancreatic and duodenal homeobox- 1(PDX-1), MafA, and β-2/Neurogenic differentiation 1 (NeuroD1) regulate insulin transcription, while the stability of preproinsulin mRNA and its untranslated regions control protein translation. Insulin secretion involves a sequence of events in β-cells that lead to fusion of secretory granules with the plasma membrane. Insulin is secreted primarily in response to glucose, while other nutrients such as free fatty acids and amino acids can augment glucose-induced insulin secretion. In addition, various hormones, such as melatonin, estrogen, leptin, growth hormone, and glucagon like peptide-1 also regulate insulin secretion. Thus, the β-cell is a metabolic hub in the body, connecting nutrient metabolism and the endocrine system. Although an increase in intracellular [Ca2+] is the primary insulin secretary signal, cAMP signaling- dependent mechanisms are also critical in the regulation of insulin secretion. This article reviews current knowledge on how β-cells synthesize and secrete insulin. In addition, this review presents evidence that genetic and environmental factors can lead to hyperglycemia, dyslipidemia, inflammation, and autoimmunity, resulting in β-cell dysfunction, thereby triggering the pathogenesis of diabetes. read more read less

Topics:

Insulin receptor substrate (71%)71% related to the paper, Insulin receptor (69%)69% related to the paper, Insulin (66%)66% related to the paper, Preproinsulin (63%)63% related to the paper, Proinsulin (62%)62% related to the paper
712 Citations
Journal Article DOI: 10.2174/1573399810602040367
Metabolic obesity: the paradox between visceral and subcutaneous fat.
Osama Hamdy1, Sriurai Porramatikul, Ebaa Al-Ozairi
01 Nov 2006 - Current Diabetes Reviews

Abstract:

In contrast to the accumulation of fat in the gluteo-femoral region, the accumulation of fat around abdominal viscera and inside intraabdominal solid organs is strongly associated with obesity-related complications like Type 2 diabetes and coronary artery disease. The association between visceral adiposity and accelerated ath... In contrast to the accumulation of fat in the gluteo-femoral region, the accumulation of fat around abdominal viscera and inside intraabdominal solid organs is strongly associated with obesity-related complications like Type 2 diabetes and coronary artery disease. The association between visceral adiposity and accelerated atherosclerosis was shown to be independent of age, overall obesity or the amount of subcutaneous fat. Recent evidence revealed several biological and genetic differences between intraabdominal visceral-fat and peripheral subcutaneous-fat. Such differences are also reflected in their contrasting roles in the pathogenesis of obesity-related cardiometabolic problems, in either lean or obese individuals. The functional differences between visceral and the subcutaneous adipocytes may be related to their anatomical location. Visceral adipose tissue and its adipose-tissue resident macrophages produce more proinflamatory cytokines like tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) and less adiponectin. These cytokines changes induce insulin resistance and play a major role in the pathogenesis of endothelial dysfunction and subsequent atherosclerosis. The rate of visceral fat accumulation is also different according to the individual's gender and ethnic background; being more prominent in white men, African American women and Asian Indian and Japanese men and women. Such differences may explain the variation in the cardiometabolic risk at different waist measurements between different populations. However, it is unclear how much visceral fat reduction is needed to induce favorable metabolic changes. On the other hand, peripheral fat mass is negatively correlated with atherogenic metabolic risk factors and its selective reduction by liposuction does improve cardiovascular risk profile. The increasing knowledge about body fat distribution and its modifiers may lead to the development of more effective treatment strategies for people with/or at high risk for Type 2 diabetes and coronary artery disease. These accumulating observations also urge our need for a new definition of obesity based on the anatomical location of fat rather than on its volume, especially when cardiometabolic risk is considered. The term "Metabolic Obesity", in reference to visceral fat accumulation in either lean or obese individuals may identify those at risk for cardiovascular disease better than the currently used definitions of obesity. read more read less

Topics:

Adipose tissue (54%)54% related to the paper, Insulin resistance (54%)54% related to the paper, Type 2 diabetes (53%)53% related to the paper, Obesity (53%)53% related to the paper, Adiponectin (53%)53% related to the paper
527 Citations
open accessOpen access Journal Article DOI: 10.2174/1573399815666191024085838
Type 2 Diabetes and its Impact on the Immune System
Afiat Berbudi1, Nofri Rahmadika1, Adi Imam Tjahjadi1, Rovina Ruslami1
01 Jan 2020 - Current Diabetes Reviews

Abstract:

Introduction: Type 2 Diabetes (T2D) is a major health problem worldwide. This metabolic disease is indicated by high blood glucose levels due to insufficient insulin production by the pancreas. An inflammatory response occurs as a result of the immune response to high blood glucose levels as well as the presence of inflammato... Introduction: Type 2 Diabetes (T2D) is a major health problem worldwide. This metabolic disease is indicated by high blood glucose levels due to insufficient insulin production by the pancreas. An inflammatory response occurs as a result of the immune response to high blood glucose levels as well as the presence of inflammatory mediators produced by adipocytes and macrophages in fat tissue. This low and chronic inflammation damages the pancreatic beta cells and leads to insufficient insulin production, which results in hyperglycemia. Hyperglycemia in diabetes is thought to cause dysfunction of the immune response, which fails to control the spread of invading pathogens in diabetic subjects. Therefore, diabetic subjects are known to more susceptible to infections. The increased prevalence of T2D will increase the incidence of infectious diseases and related comorbidities. Objective: This review provides an overview of the immunological aspect of T2D and the possible mechanisms that result in increased infections in diabetics. Conclusion: A better understanding of how immune dysfunctions occur during hyperglycemia can lead to novel treatments and preventions for infectious diseases and T2D comorbidities, thus improving the outcome of infectious disease treatment in T2D patients. read more read less

Topics:

Diabetes mellitus (58%)58% related to the paper, Type 2 diabetes (57%)57% related to the paper, Insulin (55%)55% related to the paper, Inflammation (54%)54% related to the paper, Immune system (54%)54% related to the paper
423 Citations
open accessOpen access Journal Article DOI: 10.2174/1573399810666140508121012
Leptin- and leptin receptor-deficient rodent models: relevance for human type 2 diabetes.
Bingxuan Wang, P. Charukeshi Chandrasekera, John J. Pippin1
28 Feb 2014 - Current Diabetes Reviews

Abstract:

Among the most widely used animal models in obesity-induced type 2 diabetes mellitus (T2DM) research are the congenital leptin- and leptin receptor-deficient rodent models. These include the leptin-deficient ob/ob mice and the leptin receptor-deficient db/db mice, Zucker fatty rats, Zucker diabetic fatty rats, SHR/N-cp rats, ... Among the most widely used animal models in obesity-induced type 2 diabetes mellitus (T2DM) research are the congenital leptin- and leptin receptor-deficient rodent models. These include the leptin-deficient ob/ob mice and the leptin receptor-deficient db/db mice, Zucker fatty rats, Zucker diabetic fatty rats, SHR/N-cp rats, and JCR:LA-cp rats. After decades of mechanistic and therapeutic research schemes with these animal models, many species differences have been uncovered, but researchers continue to overlook these differences, leading to untranslatable research. The purpose of this review is to analyze and comprehensively recapitulate the most common leptin/leptin receptor-based animal models with respect to their relevance and translatability to human T2DM. Our analysis revealed that, although these rodents develop obesity due to hyperphagia caused by abnormal leptin/leptin receptor signaling with the subsequent appearance of T2DM-like manifestations, these are in fact secondary to genetic mutations that do not reflect disease etiology in humans, for whom leptin or leptin receptor deficiency is not an important contributor to T2DM. A detailed comparison of the roles of genetic susceptibility, obesity, hyperglycemia, hyperinsulinemia, insulin resistance, and diabetic complications as well as leptin expression, signaling, and other factors that confound translation are presented here. There are substantial differences between these animal models and human T2DM that limit reliable, reproducible, and translatable insight into human T2DM. Therefore, it is imperative that researchers recognize and acknowledge the limitations of the leptin/leptin receptor-based rodent models and invest in research methods that would be directly and reliably applicable to humans in order to advance T2DM management. read more read less

Topics:

Leptin receptor (78%)78% related to the paper, Leptin (60%)60% related to the paper, Insulin resistance (51%)51% related to the paper
384 Citations
open accessOpen access Journal Article DOI: 10.2174/157339909788166828
Depression and quality of life in patients with diabetes: a systematic review from the European depression in diabetes (EDID) research consortium.
01 May 2009 - Current Diabetes Reviews

Abstract:

Diabetes patients are known to have a worse quality of life than individuals without diabetes. They also have an increased risk for depressive symptoms, which may have an additional negative effect on their quality of life. This systematic review summarizes the current knowledge on the association between depressive symptoms ... Diabetes patients are known to have a worse quality of life than individuals without diabetes. They also have an increased risk for depressive symptoms, which may have an additional negative effect on their quality of life. This systematic review summarizes the current knowledge on the association between depressive symptoms and quality of life in individuals with diabetes. A systematic literature search using MEDLINE, Psychinfo, Social SciSearch, SciSearch and EMBASE was conducted from January 1990 until September 2007. We identified studies that compared quality of life between diabetic individuals with and without depressive symptoms. Twenty studies were identified, including eighteen cross-sectional and two longitudinal studies. Quality of life was measured as generic, diabetes specific and domain specific quality of life. All studies reported a negative association between depressive symptoms and at least one aspect of quality of life in people with diabetes. Diabetic individuals with depressive symptoms also had a severely lower diabetes specific quality of life. Generic and domain specific quality of life were found to be mild to moderately lower in the presence of depressive symptoms. Therefore, increased awareness and monitoring for depression is needed within different diabetes care settings. read more read less

Topics:

Quality of life (healthcare) (56%)56% related to the paper, Depression (differential diagnoses) (50%)50% related to the paper, Diabetes mellitus (50%)50% related to the paper
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369 Citations
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Current Diabetes Reviews format uses Vancouver citation style.

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Frequently asked questions

1. Can I write Current Diabetes Reviews in LaTeX?

Absolutely not! Our tool has been designed to help you focus on writing. You can write your entire paper as per the Current Diabetes Reviews guidelines and auto format it.

2. Do you follow the Current Diabetes Reviews guidelines?

Yes, the template is compliant with the Current Diabetes Reviews 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 Current Diabetes Reviews?

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 Current Diabetes Reviews citation style.

4. Can I use the Current Diabetes Reviews templates for free?

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 Current Diabetes Reviews.

5. Can I use a manuscript in Current Diabetes Reviews that I have written in MS Word?

Yes. You can choose the right template, copy-paste the contents from the word document, and click on auto-format. Once you're done, you'll have a publish-ready paper Current Diabetes Reviews that you can download at the end.

6. How long does it usually take you to format my papers in Current Diabetes Reviews?

It only takes a matter of seconds to edit your manuscript. Besides that, our intuitive editor saves you from writing and formatting it in Current Diabetes Reviews.

7. Where can I find the template for the Current Diabetes Reviews?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Current Diabetes Reviews's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

8. Can I reformat my paper to fit the Current Diabetes Reviews's guidelines?

Of course! You can do this using our intuitive editor. It's very easy. If you need help, our support team is always ready to assist you.

9. Current Diabetes Reviews an online tool or is there a desktop version?

SciSpace's Current Diabetes Reviews is currently available as an online tool. We're developing a desktop version, too. You can request (or upvote) any features that you think would be helpful for you and other researchers in the "feature request" section of your account once you've signed up with us.

10. I cannot find my template in your gallery. Can you create it for me like Current Diabetes Reviews?

Sure. You can request any template and we'll have it setup within a few days. You can find the request box in Journal Gallery on the right side bar under the heading, "Couldn't find the format you were looking for like Current Diabetes Reviews?”

11. What is the output that I would get after using Current Diabetes Reviews?

After writing your paper autoformatting in Current Diabetes Reviews, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is Current Diabetes Reviews'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 Current Diabetes Reviews?

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 Current Diabetes Reviews. 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 Current Diabetes Reviews?

The 5 most common citation types in order of usage for Current Diabetes Reviews are:.

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

15. How do I submit my article to the Current Diabetes Reviews?

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16. Can I download Current Diabetes Reviews in Endnote format?

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 Current Diabetes Reviews Endnote style according to Elsevier guidelines.

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