Example of Diabetes, Obesity and Metabolism format
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Example of Diabetes, Obesity and Metabolism format Example of Diabetes, Obesity and Metabolism format Example of Diabetes, Obesity and Metabolism format Example of Diabetes, Obesity and Metabolism format Example of Diabetes, Obesity and Metabolism format Example of Diabetes, Obesity and Metabolism format Example of Diabetes, Obesity and Metabolism format
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Diabetes, Obesity and Metabolism — Template for authors

Publisher: Wiley
Categories Rank Trend in last 3 yrs
Endocrinology, Diabetes and Metabolism #14 of 219 down down by 2 ranks
Endocrinology #8 of 117 down down by 2 ranks
Internal Medicine #9 of 121 down down by 1 rank
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 1213 Published Papers | 13183 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 18/06/2020
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Related Journals

open access Open Access

Springer

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

Elsevier

Quality:  
High
CiteRatio: 5.4
SJR: 1.022
SNIP: 1.091
open access Open Access

Elsevier

Quality:  
High
CiteRatio: 7.7
SJR: 1.605
SNIP: 2.01
open access Open Access

Wiley

Quality:  
High
CiteRatio: 6.1
SJR: 1.474
SNIP: 1.473

Journal Performance & Insights

Impact Factor

CiteRatio

Determines the importance of a journal by taking a measure of frequency with which the average article in a journal has been cited in a particular year.

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

5.9

4% from 2018

Impact factor for Diabetes, Obesity and Metabolism from 2016 - 2019
Year Value
2019 5.9
2018 6.133
2017 5.98
2016 6.715
graph view Graph view
table view Table view

10.9

15% from 2019

CiteRatio for Diabetes, Obesity and Metabolism from 2016 - 2020
Year Value
2020 10.9
2019 9.5
2018 9.3
2017 11.8
2016 14.0
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has decreased by 4% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 15% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

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.

2.445

2% from 2019

SJR for Diabetes, Obesity and Metabolism from 2016 - 2020
Year Value
2020 2.445
2019 2.497
2018 2.777
2017 2.842
2016 3.072
graph view Graph view
table view Table view

1.479

1% from 2019

SNIP for Diabetes, Obesity and Metabolism from 2016 - 2020
Year Value
2020 1.479
2019 1.499
2018 1.656
2017 1.638
2016 1.729
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has decreased by 2% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has decreased by 1% in last years.
  • This journal’s SNIP is in the top 10 percentile category.
Diabetes, Obesity and Metabolism

Guideline source: View

All company, product and service names used in this website are for identification purposes only. All product names, trademarks and registered trademarks are property of their respective owners.

Use of these names, trademarks and brands does not imply endorsement or affiliation. Disclaimer Notice

Wiley

Diabetes, Obesity and Metabolism

Diabetes, Obesity & Metabolism is primarily a journal of clinical and experimental pharmacology and therapeutics covering the interrelated areas of diabetes, obesity and metabolism. The journal prioritises high-quality original research that reports on the effects of new or ex...... Read More

Medicine

i
Last updated on
17 Jun 2020
i
ISSN
1462-8902
i
Impact Factor
High - 1.735
i
Acceptance Rate
25%
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
Yellow faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
apa
i
Citation Type
Numbered
[25]
i
Bibliography Example
Beenakker, C.W.J. (2006) Specular andreev reflection in graphene.Phys. Rev. Lett., 97 (6), 067 007. URL 10.1103/PhysRevLett.97.067007.

Top papers written in this journal

Journal Article DOI: 10.1111/J.1463-1326.2008.00969.X
Pancreatic beta-cell mass in European subjects with type 2 diabetes.
Jacques Rahier1, Yves Guiot1, Rose-Marie Goebbels1, Christine Sempoux1, Jean-Claude Henquin1

Abstract:

Decreases in both beta-cell function and number can contribute to insulin deficiency in type 2 diabetes. Here, we quantified the beta-cell mass in pancreas obtained at autopsy of 57 type 2 diabetic (T2D) and 52 non-diabetic subjects of European origin. Sections from the body and tail were immunostained for insulin. The beta-c... Decreases in both beta-cell function and number can contribute to insulin deficiency in type 2 diabetes. Here, we quantified the beta-cell mass in pancreas obtained at autopsy of 57 type 2 diabetic (T2D) and 52 non-diabetic subjects of European origin. Sections from the body and tail were immunostained for insulin. The beta-cell mass was calculated from the volume density of beta-cells (measured by point-counting methods) and the weight of the pancreas. The pancreatic insulin concentration was measured in some of the subjects. beta-cell mass increased only slightly with body mass index (BMI). After matching for BMI, the beta-cell mass was 41% (BMI 15 years of overt diabetes respectively). Pancreatic insulin concentration was 30% lower in patients. In conclusion, the average beta-cell mass is about 39% lower in T2D subjects compared with matched controls. Its decrease with duration of the disease could be a consequence of diabetes that, with further impairment of insulin secretion, contributes to the progressive deterioration of glucose homeostasis. We do not believe that the small difference in beta-cell mass observed within 5 years of onset could cause diabetes in the absence of beta-cell dysfunction. read more read less

Topics:

Type 2 diabetes (61%)61% related to the paper, Diabetes mellitus (59%)59% related to the paper, Insulin (58%)58% related to the paper, Body mass index (56%)56% related to the paper, Glucose homeostasis (54%)54% related to the paper
View PDF
706 Citations
Journal Article DOI: 10.1111/J.1463-1326.2006.00704.X
Efficacy and safety of the dipeptidyl peptidase‐4 inhibitor, sitagliptin, compared with the sulfonylurea, glipizide, in patients with type 2 diabetes inadequately controlled on metformin alone: a randomized, double‐blind, non‐inferiority trial
M. A. Nauck, G. Meininger1, D. Sheng1, L. Terranella1, Peter P. Stein1

Abstract:

Aim: To compare the efficacy and safety of sitagliptin vs glipizide in patients with type 2 diabetes and inadequate glycaemic control [haemoglobin A1c (HbA1c) ≥ 65 and ≤10%] on metformin monotherapy Methods:  After a metformin dose titration/stabilization period (≥1500 mg/day), 1172 patients were randomized to the addition... Aim: To compare the efficacy and safety of sitagliptin vs glipizide in patients with type 2 diabetes and inadequate glycaemic control [haemoglobin A1c (HbA1c) ≥ 65 and ≤10%] on metformin monotherapy Methods:  After a metformin dose titration/stabilization period (≥1500 mg/day), 1172 patients were randomized to the addition of sitagliptin 100 mg qd (N = 588) or glipizide 5 mg/day (uptitrated to a potential maximum 20 mg/day) (N = 584) for 52 weeks The primary analysis assessed whether sitagliptin was non-inferior to glipizide regarding HbA1c changes from baseline at Week 52 using a per-protocol approach Results:  From a mean baseline of 75%, HbA1c changes from baseline were −067% at Week 52 in both groups, confirming non-inferiority The proportions achieving an HbA1c < 7% were 63% (sitagliptin) and 59% (glipizide) Fasting plasma glucose changes from baseline were −056 mmol/l (−100 mg/dl) and −042 mmol/l (−75 mg/dl) for sitagliptin and glipizide, respectively The proportion of patients experiencing hypoglycaemia episodes was significantly (p < 0001) higher with glipizide (32%) than with sitagliptin (5%), with 657 events in glipizide-treated patients compared with 50 events in sitagliptin-treated patients Sitagliptin led to weight loss (change from baseline =−15 kg) compared with weight gain (+11 kg) with glipizide [between-treatment difference (95% confidence interval) =−25 kg (−31, −20); p < 0001] Conclusions:  In this study, the addition of sitagliptin compared with glipizide provided similar HbA1c-lowering efficacy over 52 weeks in patients on ongoing metformin therapy Sitagliptin was generally well tolerated, with a lower risk of hypoglycaemia relative to glipizide and with weight loss compared with weight gain with glipizide read more read less

Topics:

Glipizide (64%)64% related to the paper, Sitagliptin (62%)62% related to the paper, Sitagliptin Phosphate (61%)61% related to the paper, Dipeptidyl peptidase-4 inhibitor (54%)54% related to the paper, Metformin (51%)51% related to the paper
View PDF
673 Citations
open accessOpen access Journal Article DOI: 10.1111/DOM.12127
Dapagliflozin a glucose-regulating drug with diuretic properties in subjects with type 2 diabetes.
H. J. Lambers Heerspink1, Dick de Zeeuw1, L. Wie, B. Leslie2, J. List2

Abstract:

Aims Sodium–glucose co-transporter 2 (SGLT2) reabsorbs glucose and sodium in the renal proximal tubule. Dapagliflozin, an SGLT2 inhibitor, targets hyperglycaemia in type 2 diabetes by increasing renal glucose excretion. To investigate whether the parallel occurring sodium loss would have diuretic-like physiologic effects, we... Aims Sodium–glucose co-transporter 2 (SGLT2) reabsorbs glucose and sodium in the renal proximal tubule. Dapagliflozin, an SGLT2 inhibitor, targets hyperglycaemia in type 2 diabetes by increasing renal glucose excretion. To investigate whether the parallel occurring sodium loss would have diuretic-like physiologic effects, we compared dapagliflozin and hydrochlorothiazide (HCTZ) effects on 24-h blood pressure (BP), body weight, plasma volume and glomerular filtration rate (GFR). Methods In this randomized, placebo-controlled, double-blind trial, 75 subjects with type 2 diabetes were assigned placebo, dapagliflozin 10 mg/day, or HCTZ 25 mg/day. Changes from baseline BP, body weight, plasma volume and GFR were assessed after 12 weeks of treatment. Results Subjects' mean age was 56 years, type 2 diabetes mellitus (T2DM) duration 6.3 years, and haemoglobin A1c (HbA1c) 7.5%. Treatment with placebo, dapagliflozin or HCTZ resulted in changes from baseline in 24-h ambulatory mean systolic blood pressure (SBP) of −0.9 (95%CI −4.2, +2.4), −3.3 (95%CI −6.8, +0.2), and −6.6 (95%CI −9.9, −3.2) mmHg, respectively at week 12, adjusted for baseline SBP. Body weight decreased with dapagliflozin and HCTZ. In a sub-study plasma volume appeared to decrease with dapagliflozin but did not change with placebo or HCTZ treatment. Dapagliflozin induced a greater reduction in GFR (−10.8%; 95%CI −14.6, −6.7) relative to placebo (−2.9%; 95% CI −6.9, +1.2) or HCTZ (−3.4%; 95%CI −7.3, +0.6). Conclusions Dapagliflozin-induced SGLT2 inhibition for 12 weeks is associated with reductions in 24-h BP, body weight, GFR and possibly plasma volume. Cumulatively, these effects suggest that dapagliflozin may have a diuretic-like capacity to lower BP in addition to beneficial effects on glycaemic control. read more read less

Topics:

Dapagliflozin (68%)68% related to the paper, Hydrochlorothiazide (54%)54% related to the paper, Renal function (51%)51% related to the paper, Type 2 diabetes (50%)50% related to the paper
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616 Citations
Journal Article DOI: 10.1111/J.1463-1326.2005.00510.X
Adiponectin--a key adipokine in the metabolic syndrome.

Abstract:

Adiponectin is a recently described adipokine that has been recognized as a key regulator of insulin sensitivity and tissue inflammation. It is produced by adipose tissue (white and brown) and circulates in the blood at very high concentrations. It has direct actions in liver, skeletal muscle and the vasculature, with promine... Adiponectin is a recently described adipokine that has been recognized as a key regulator of insulin sensitivity and tissue inflammation. It is produced by adipose tissue (white and brown) and circulates in the blood at very high concentrations. It has direct actions in liver, skeletal muscle and the vasculature, with prominent roles to improve hepatic insulin sensitivity, increase fuel oxidation [via up-regulation of adenosine monophosphate-activated protein kinase (AMPK) activity] and decrease vascular inflammation. Adiponectin exists in the circulation as varying molecular weight forms, produced by multimerization. Recent data indicate that the high-molecular weight (HMW) complexes have the predominant action in the liver. In contrast to other adipokines, adiponectin secretion and circulating levels are inversely proportional to body fat content. Levels are further reduced in subjects with diabetes and coronary artery disease. Adiponectin antagonizes many effects of tumour necrosis factor-alpha(TNF-alpha) and this, in turn, suppresses adiponectin production. Furthermore, adiponectin secretion from adipocytes is enhanced by thiazolidinediones (which also act to antagonize TNF-alpha effects). Thus, adiponectin may be the common mechanism by which TNF-alpha promotes, and the thiazolidinediones suppress, insulin resistance and inflammation. Two adiponectin receptors, termed AdipoR1 and AdipoR2, have been identified and these are ubiquitously expressed. AdipoR1 is most highly expressed in skeletal muscle and has a prominent action to activate AMPK, and hence promote lipid oxidation. AdipoR2 is most highly expressed in liver, where it enhances insulin sensitivity and reduces steatosis via activation of AMPK and increased peroxisome-proliferator-activated receptor alpha ligand activity. T-cadherin, which is expressed in endothelium and smooth muscle, has been identified as an adiponectin-binding protein with preference for HMW adiponectin multimers. Given the low levels of adiponectin in subjects with the metabolic syndrome, and the beneficial effect of the adipokine in animal studies, there is exciting potential for adiponectin replacement therapy in insulin resistance and related disorders. read more read less

Topics:

Adiponectin secretion (76%)76% related to the paper, Adiponectin (68%)68% related to the paper, Adipokine (61%)61% related to the paper, Insulin resistance (57%)57% related to the paper, AMPK (55%)55% related to the paper
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604 Citations
Journal Article DOI: 10.1111/J.1463-1326.2010.01275.X
Hepatic steatosis: a role for de novo lipogenesis and the transcription factor SREBP-1c
Pascal Ferré1, Fabienne Foufelle1

Abstract:

Steatosis is an accumulation of triglycerides in the liver. Although an excessive availability of plasma fatty acids is an important determinant of steatosis, lipid synthesis from glucose (lipogenesis) is now also considered as an important contributing factor. Lipogenesis is an insulin- and glucose-dependent process that is ... Steatosis is an accumulation of triglycerides in the liver. Although an excessive availability of plasma fatty acids is an important determinant of steatosis, lipid synthesis from glucose (lipogenesis) is now also considered as an important contributing factor. Lipogenesis is an insulin- and glucose-dependent process that is under the control of specific transcription factors, sterol regulatory element binding protein 1c (SREBP-1c), activated by insulin and carbohydrate response element binding protein (ChREBP) activated by glucose. Insulin induces the maturation of SREBP-1c by a proteolytic mechanism initiated in the endoplasmic reticulum (ER). SREBP-1c in turn activates glycolytic gene expression, allowing glucose metabolism, and lipogenic genes in conjunction with ChREBP. Lipogenesis activation in the liver of obese markedly insulin-resistant steatotic rodents is then paradoxical. Recent data suggest that the activation of SREBP-1c and thus of lipogenesis is secondary in the steatotic liver to an ER stress. The ER stress activates the cleavage of SREBP-1c independent of insulin, thus explaining the paradoxical stimulation of lipogenesis in an insulin-resistant liver. Inhibition of the ER stress in obese rodents decreases SREBP-1c activation and lipogenesis and improves markedly hepatic steatosis and insulin sensitivity. ER is thus a new partner in steatosis and metabolic syndrome which is worth considering as a potential therapeutic target. read more read less

Topics:

Lipogenesis (67%)67% related to the paper, Steatosis (56%)56% related to the paper, Insulin resistance (56%)56% related to the paper, Fatty liver (56%)56% related to the paper, Insulin (54%)54% related to the paper
View PDF
578 Citations
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Diabetes, Obesity and Metabolism format uses apa citation style.

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Frequently asked questions

1. Can I write Diabetes, Obesity and Metabolism in LaTeX?

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

2. Do you follow the Diabetes, Obesity and Metabolism guidelines?

Yes, the template is compliant with the Diabetes, Obesity and 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 Diabetes, Obesity and 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 Diabetes, Obesity and Metabolism citation style.

4. Can I use the Diabetes, Obesity and Metabolism 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 Diabetes, Obesity and Metabolism.

5. Can I use a manuscript in Diabetes, Obesity and Metabolism 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 Diabetes, Obesity and Metabolism that you can download at the end.

6. How long does it usually take you to format my papers in Diabetes, Obesity and Metabolism?

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

7. Where can I find the template for the Diabetes, Obesity and Metabolism?

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 Diabetes, Obesity and Metabolism'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 Diabetes, Obesity and Metabolism'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. Diabetes, Obesity and Metabolism an online tool or is there a desktop version?

SciSpace's Diabetes, Obesity and Metabolism 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 Diabetes, Obesity and Metabolism?

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 Diabetes, Obesity and Metabolism?”

11. What is the output that I would get after using Diabetes, Obesity and Metabolism?

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

12. Is Diabetes, Obesity and 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 Diabetes, Obesity and 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 Diabetes, Obesity and 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 Diabetes, Obesity and Metabolism?

The 5 most common citation types in order of usage for Diabetes, Obesity and Metabolism 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 Diabetes, Obesity and Metabolism?

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16. Can I download Diabetes, Obesity and Metabolism 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 Diabetes, Obesity and Metabolism Endnote style according to Elsevier guidelines.

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I spent hours with MS word for reformatting. It was frustrating - plain and simple. With SciSpace, I can draft my manuscripts and once it is finished I can just submit. In case, I have to submit to another journal it is really just a button click instead of an afternoon of reformatting.

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