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Type 2 Diabetes-II: Pathogenesis, Diagnosis, and Treatment

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (31 March 2020) | Viewed by 13633

Special Issue Editor


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Guest Editor
Graduate School of Medical Science, Department of Endocrinology and Metabolism, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
Interests: chronic inflammation; non-alcoholic fatty liver disease; intestinal microbiota; diabetes; nutrition; artificial in-telligence; metabolism
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Special Issue Information

Dear Colleagues,

Recently, attempts to understand the type 2 diabetes, a pathological condition of sarcopenic obesity involving a decrease in skeletal muscle mass combined with an increase in visceral fat, have attracted attention.

The term “sarcopenia” was coined in 1988 by Dr. Irwin Rosenberg as age-related loss of skeletal muscle mass and skeletal muscle strength. At present, loss of skeletal muscle mass and skeletal muscle strength in various pathological conditions other than aging is regarded as important.

On the other hand, metabolic abnormalities, which occur with abdominal obesity or ectopic fat and are associated with diabetes, fatty liver, and cardiovascular diseases, now focus on the relationship with sarcopenia. In addition, many non-obese people with metabolic abnormalities, who are not obese according to their BMI, have been developing type 2 diabetes in Asia. These metabolic abnormalities are thought to be a cause of sarcopenic obesity, but the pathological condition has not been clarified yet. Moreover, treatment for sarcopenic obesity has also not been established.

This Special Issue aims to provide a forum for the dissemination of the latest information on pathogenesis, and treatment for sarcopenic obesity.

Prof. Dr. Masahide Hamaguchi
Guest Editor

Manuscript Submission Information

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Keywords

  • Sarcopenia
  • Obesity
  • Lean
  • Sarcopenic obesity
  • Fatty liver
  • Diabetes

Published Papers (3 papers)

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Research

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9 pages, 846 KiB  
Article
A Pilot Study on the Effect of Anti-Thrombopoietin Antibody on Platelet Count in Patients with Type 2 Diabetes
by Takuya Fukuda, Masahide Hamaguchi, Takafumi Osaka, Yoshitaka Hashimoto, Emi Ushigome, Mai Asano, Masahiro Yamazaki, Eriko Fukuda, Kei Yamaguchi, Koji Ogawa, Naoki Goshima and Michiaki Fukui
Molecules 2020, 25(7), 1667; https://doi.org/10.3390/molecules25071667 - 4 Apr 2020
Cited by 2 | Viewed by 2312
Abstract
Thrombopoietin (THPO) is a circulatory cytokine that plays an important role in platelet production. The presence of anti-THPO antibody relates to thrombocytopenia and is rarely seen in hematopoietic and autoimmune diseases. To date, there had been no reports that focused on the anti-THPO [...] Read more.
Thrombopoietin (THPO) is a circulatory cytokine that plays an important role in platelet production. The presence of anti-THPO antibody relates to thrombocytopenia and is rarely seen in hematopoietic and autoimmune diseases. To date, there had been no reports that focused on the anti-THPO antibody in patients with type 2 diabetes mellitus (T2DM). To evaluate prevalence of the anti-THPO antibody in patients with T2DM and the relationship between anti-THPO antibody and platelet count, a cross-sectional study was performed on 82 patients with T2DM. The anti-THPO antibody was measured by ELISA using preserved sera and detected in 13 patients. The average platelet count was significantly lower in patients with the anti-THPO antibody than in those without the anti-THPO antibody. Multivariate linear regression analyses showed a significant relationship between the anti-THPO antibody and platelet count, after adjusting for other variables. To our best knowledge, this was the first report on the effect of the anti-THPO antibody on platelet count in patients with T2DM. Further investigation is needed to validate the prevalence and pathological significance of the anti-THPO antibody in patients with T2DM. Full article
(This article belongs to the Special Issue Type 2 Diabetes-II: Pathogenesis, Diagnosis, and Treatment)
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12 pages, 1099 KiB  
Article
Exercise Affects Blood Glucose Levels and Tissue Chromium Distribution in High-Fat Diet-Fed C57BL6 Mice
by Geng-Ruei Chang, Po-Hsun Hou, Wen-Kai Chen, Chien-Teng Lin, Hsiao-Pei Tsai and Frank Chiahung Mao
Molecules 2020, 25(7), 1658; https://doi.org/10.3390/molecules25071658 - 3 Apr 2020
Cited by 25 | Viewed by 4149
Abstract
Obesity is commonly associated with hyperglycemia and type 2 diabetes and negatively affects chromium accumulation in tissues. Exercise prevents and controls obesity and type 2 diabetes. However, little information is available regarding chromium changes for regulating glucose homeostasis in high-fat diet (HFD)-fed animals/humans [...] Read more.
Obesity is commonly associated with hyperglycemia and type 2 diabetes and negatively affects chromium accumulation in tissues. Exercise prevents and controls obesity and type 2 diabetes. However, little information is available regarding chromium changes for regulating glucose homeostasis in high-fat diet (HFD)-fed animals/humans who exercise. Therefore, this study explored the effects of exercise and whether it alters chromium distribution in obese mice. Male C57BL6/J mice aged 4 weeks were randomly divided into two groups and fed either an HFD or standard diet (SD). Each group was subgrouped into two additional groups in which one subgroup was exposed to treadmill exercise for 12 weeks and the other comprised control mice. HFD-fed mice that exercised exhibited significant lower body weight gain, food/energy intake, daily food efficiency, and serum leptin and insulin levels than did HFD-fed control mice. Moreover, exercise reduced fasting glucose and enhanced insulin sensitivity and pancreatic β-cell function, as determined by homeostasis model assessment (HOMA)-insulin resistance and HOMA-β indices, respectively. Exercise also resulted in markedly higher chromium levels within the muscle, liver, fat tissues, and kidney but lower chromium levels in the bone and bloodstream in obese mice than in control mice. However, these changes were not noteworthy in SD-fed mice that exercised. Thus, exercise prevents and controls HFD-induced obesity and may modulate chromium distribution in insulin target tissues. Full article
(This article belongs to the Special Issue Type 2 Diabetes-II: Pathogenesis, Diagnosis, and Treatment)
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Review

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32 pages, 943 KiB  
Review
Anti-Inflammatory Strategies Targeting Metaflammation in Type 2 Diabetes
by Alina Kuryłowicz and Krzysztof Koźniewski
Molecules 2020, 25(9), 2224; https://doi.org/10.3390/molecules25092224 - 9 May 2020
Cited by 55 | Viewed by 6750
Abstract
One of the concepts explaining the coincidence of obesity and type 2 diabetes (T2D) is the metaflammation theory. This chronic, low-grade inflammatory state originating from metabolic cells in response to excess nutrients, contributes to the development of T2D by increasing insulin resistance in [...] Read more.
One of the concepts explaining the coincidence of obesity and type 2 diabetes (T2D) is the metaflammation theory. This chronic, low-grade inflammatory state originating from metabolic cells in response to excess nutrients, contributes to the development of T2D by increasing insulin resistance in peripheral tissues (mainly in the liver, muscles, and adipose tissue) and by targeting pancreatic islets and in this way impairing insulin secretion. Given the role of this not related to infection inflammation in the development of both: insulin resistance and insulitis, anti-inflammatory strategies could be helpful not only to control T2D symptoms but also to treat its causes. This review presents current concepts regarding the role of metaflammation in the development of T2D in obese individuals as well as data concerning possible application of different anti-inflammatory strategies (including lifestyle interventions, the extra-glycemic potential of classical antidiabetic compounds, nonsteroidal anti-inflammatory drugs, immunomodulatory therapies, and bariatric surgery) in the management of T2D. Full article
(This article belongs to the Special Issue Type 2 Diabetes-II: Pathogenesis, Diagnosis, and Treatment)
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