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Obesity and Hormones

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A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (30 June 2019) | Viewed by 34977

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Dr. Srinivas Nammi

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Guest Editor

Discipline of Medical Sciences, School of Science and NICM-Health Research Institute, Western Sydney University, Sydney, NSW 2751, Australia
Interests: obesity; metabolic syndrome; diabetes; dyslipidaemia; fatty liver disease; chronic kidney disease

Special Issue Information

Dear Colleagues,

Obesity is a complex multi-factorial chronic medical condition characterized by overweight with excess or abnormal body fat accumulation. It is considered as a strong risk factor in the development of serious diseases, such as type 2 diabetes, hypertension, cardiovascular disease, stroke, gastrointestinal disorders, and certain cancers. In general, obesity is caused by increased intake of energy rich foods and/or decreased exercise and physical activity. Among the genetic factors, hormonal imbalance as a cause and consequence of obesity play a role with adverse health effects of obesity. Several hormones, including insulin, leptin, sex hormones and growth hormone, have been studied extensively and play a role in appetite, metabolism, body fat distribution and increased storage of excess energy as fats. Thus, excess or deficit of hormones leads to obesity and, on the other hand, obesity also results in changes in certain hormones that contribute to the adverse metabolic effects of obesity leading to life-threatening chronic diseases. Although past research in understanding the etiology of hormonal imbalance as a cause of obesity, recent technological and analytical advances have enabled detection of a number of obesity susceptible genes involved in the regulation of food intake and in adipocyte function. These results provide plausible biological pathways that may be targeted in the future as part of treatment or prevention strategies.

We invite scientists to contribute both original research articles or reviews covering studies on hormonal intervention on obesity and its complications. Both basic and translational research papers are welcome.

Dr. Srinivas Nammi
Guest Editor

Manuscript Submission Information

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Keywords

obesity
leptin
insulin
estrogens
androgens
growth hormone

Published Papers (7 papers)

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Research

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20 pages, 3882 KiB

Open AccessArticle

Differential Sympathetic Activation of Adipose Tissues by Brain-Derived Neurotrophic Factor

by Qi Zhu, Xian Liu, Bradley J. Glazier, Kristen N. Krolick, Shangyuwen Yang, Jingyan He, Chunmin C. Lo and Haifei Shi

Biomolecules 2019, 9(9), 452; https://doi.org/10.3390/biom9090452 - 05 Sep 2019

Cited by 13 | Viewed by 3720

Abstract

Centrally administered brain-derived neurotrophic factor (BDNF) decreases body adiposity beyond what can be accounted for by decreased food intake, implying enhanced lipid metabolism by BDNF. Consistent with this notion, intracerebroventricular (icv) injection of BDNF in rats increased the expression of lipolytic enzymes in white adipose tissues (WAT) and increased circulating concentrations of lipolytic products without changing the levels of adrenal gland hormones. This suggests that central BDNF-induced lipid mobilization is likely due to sympathetic neural activation, rather than activation of the adrenocortical or adrenomedullary system. We hypothesized that BDNF activated sympathetic innervation of adipose tissues to regulate lipolysis. Rats with unilateral denervation of interscapular brown adipose tissue (BAT) and different WAT depots received icv injections of saline or BDNF. Both intact and denervated adipose tissues were exposed to the same circulating factors, but denervated adipose tissues did not receive neural signals. Norepinephrine (NE) turnover (NETO) of BAT and WAT was assessed as a measure of sympathetic activity. Findings revealed that central BDNF treatment induced a change in NETO in some but not all the adipose tissues tested. Specifically, greater NETO rates were found in BAT and gonadal epididymal WAT (EWAT), but not in inguinal WAT (IWAT) or retroperitoneal WAT (RWAT), of BDNF-treated rats compared to saline-treated rats. Furthermore, intact innervation was necessary for BDNF-induced NETO in BAT and EWAT. In addition, BDNF increased the expression of lipolytic enzymes in both intact and denervated EWAT and IWAT, suggesting that BDNF-induced WAT lipolysis was independent of intact innervation. To summarize, centrally administered BDNF selectively provoked sympathetic drives to BAT and EWAT that was dependent on intact innervation, while BDNF also increased lipolysis in a manner independent of intact innervation. Full article

(This article belongs to the Special Issue Obesity and Hormones)

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12 pages, 2086 KiB

Open AccessArticle

Superiority of the Non-Glycosylated Form over the Glycosylated Form of Irisin in the Attenuation of Adipocytic Meta-Inflammation: A Potential Factor in the Fight against Insulin Resistance

by Agnieszka Irena Mazur-Bialy

Biomolecules 2019, 9(9), 394; https://doi.org/10.3390/biom9090394 - 21 Aug 2019

Cited by 17 | Viewed by 3060

Abstract

Irisin is an adipomyokine that promotes the browning of white adipose tissue and exhibits protective potential against the development of insulin resistance and type 2 diabetes. In our bodies, it occurs in its glycosylated form (G-IR): its activity is still poorly understood, because the majority of studies have used its non-glycosylated counterpart (nG-IR). Glycosylation can affect protein function: therefore, the present study attempted to compare the actions of both forms of irisin toward inflammatory activation of the main component of adipose tissue. The study was carried out in a coculture of 3T3 adipocytes and RAW 264.7 macrophages maintained in the presence of nG-IR or G-IR. The impact on vitality and the expression and release of key inflammatory mediators important for insulin resistance and diabetes development were assessed. The studies showed that both forms effectively inhibited the expression and release of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, macrophage chemotactic protein (MCP)-1, high-mobility group box (HMGB1), leptin, and adiponectin. However, in the case of TNF-α, IL-1β, MCP-1, and HMGB1, the inhibition exerted by nG-IR was more prominent than that by G-IR. In addition, only nG-IR significantly inhibited macrophage migration. Here, nG-IR seemed to be the stronger inhibitor of the development of obesity-related inflammation; however, G-IR also had anti-inflammatory potential. Full article

(This article belongs to the Special Issue Obesity and Hormones)

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8 pages, 1157 KiB

Open AccessCommunication

tRNA-Derived Small Non-Coding RNAs as Novel Epigenetic Molecules Regulating Adipogenesis

by Linyuan Shen, Zhendong Tan, Mailin Gan, Qiang Li, Lei Chen, Lili Niu, Dongmei Jiang, Ye Zhao, Jinyong Wang, Xuewei Li, Shunhua Zhang and Li Zhu

Biomolecules 2019, 9(7), 274; https://doi.org/10.3390/biom9070274 - 11 Jul 2019

Cited by 38 | Viewed by 5813

Abstract

tRNA-derived fragments (tRFs), a novel type of non-coding RNA derived from tRNAs, play an important part in governing gene expressions at a post-transcriptional level. To date, the regulatory mechanism of tRFs governing fat deposition and adipogenesis is completely unknown. In this study, high fat diet was employed to induce an obese rat model, and tRFs transcriptome sequencing was conducted to identify differentially expressed tRFs that response to obesity. We found out that tRF^GluTTC, which promoted preadipocyte proliferation by increasing expressions of cell cycle regulatory factors, had the highest fold change in the 296 differentially expressed tRFs. Moreover, tRF^GluTTC also suppressed preadipocyte differentiation by reducing triglyceride content and lipid accumulation, and by decreasing expressions of genes that related to fatty acid synthesis. According to results of luciferase activity analysis, tRF^GluTTC directly targeted Kruppel-like factor (KLF) 9, KLF11, and KLF12, thus significantly suppressing mRNA expressions of these target genes. Moreover, tRF^GluTTC suppressed adipogenesis, accompanying by suppressing expressions of adipogenic transcription factors (aP2, PPARγ, and C/EBPα). In conclusion, these results imply that tRF^GluTTC may act as a novel epigenetic molecule regulating adipogenesis and could provide a new strategy for the intervention treatment of obesity. Full article

(This article belongs to the Special Issue Obesity and Hormones)

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12 pages, 1013 KiB

Open AccessArticle

The Relationship between Epicardial Adipose Tissue Thickness and Serum Interleukin-17a Level in Patients with Isolated Metabolic Syndrome

by Esra Demir, Nazmiye Özlem Harmankaya, İrem Kıraç Utku, Gönül Açıksarı, Turgut Uygun, Hanise Özkan and Bülent Demir

Biomolecules 2019, 9(3), 97; https://doi.org/10.3390/biom9030097 - 11 Mar 2019

Cited by 11 | Viewed by 2957

Abstract

In this study, it was aimed to investigate the relationship between the epicardial adipose tissue thickness (EATT) and serum IL-17A level insulin resistance in metabolic syndrome patients. This study enrolled a total of 160 subjects, of whom 80 were consecutive patients who applied to our outpatient clinic and were diagnosed with metabolic syndrome, and the other 80 were consecutive patients who were part of the control group with similar age and demographics in whom the metabolic syndrome was excluded. The metabolic syndrome diagnosis was made according to International Diabetes Federation (IDF)-2005 criteria. EATT was measured with transthoracic echocardiography (TTE) in the subjects. IL-17A serum levels were determined using the ELISA method. Fasting blood glucose, HDL, triglyceride, and fasting insulin levels were significantly higher in the metabolic syndrome group compared to the control group. In addition, the metabolic syndrome group had significantly higher high-sensitivity C-reactive protein (hs-CRP) and Homeostatic Model Assessment Insulin Resistance (HOMA-IR) levels than the control group. Similarly, serum IL-17A levels were significantly elevated in the metabolic syndrome group compared to the control group statistically (p < 0.001). As well, EATT was higher in the metabolic syndrome than the control group. Conclusion: By virtue of their proinflammatory properties, EATT and IL-17 may play an important role in the pathogenesis of the metabolic syndrome. Full article

(This article belongs to the Special Issue Obesity and Hormones)

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21 pages, 7193 KiB

Open AccessArticle

Integrative Analyses of Genes Associated with Subcutaneous Insulin Resistance

by Manoj Kumar Pujar, Basavaraj Vastrad and Chanabasayya Vastrad

Biomolecules 2019, 9(2), 37; https://doi.org/10.3390/biom9020037 - 22 Jan 2019

Cited by 14 | Viewed by 5240

Abstract

Insulin resistance is present in the majority of patients with non-insulin-dependent diabetes mellitus (NIDDM) and obesity. In this study, we aimed to investigate the key genes and potential molecular mechanism in insulin resistance. Expression profiles of the genes were extracted from the Gene Expression Omnibus (GEO) database. Pathway and Gene Ontology (GO) enrichment analyses were conducted at Enrichr. The protein–protein interaction (PPI) network was settled and analyzed using the Search Tool for the Retrieval of Interacting Genes (STRING) database constructed by Cytoscape software. Modules were extracted and identified by the PEWCC1 plugin. The microRNAs (miRNAs) and transcription factors (TFs) which control the expression of differentially expressed genes (DEGs) were analyzed using the NetworkAnalyst algorithm. A database (GSE73108) was downloaded from the GEO databases. Our results identified 873 DEGs (435 up-regulated and 438 down-regulated) genetically associated with insulin resistance. The pathways which were enriched were pathways in complement and coagulation cascades and complement activation for up-regulated DEGs, while biosynthesis of amino acids and the Notch signaling pathway were among the down-regulated DEGs. Showing GO enrichment were cardiac muscle cell–cardiac muscle cell adhesion and microvillus membrane for up-regulated DEGs and negative regulation of osteoblast differentiation and dendrites for down-regulated DEGs. Subsequently, myosin VB (MYO5B), discs, large homolog 2(DLG2), axin 2 (AXIN2), protein tyrosine kinase 7 (PTK7), Notch homolog 1 (NOTCH1), androgen receptor (AR), cyclin D1 (CCND1) and Rho family GTPase 3 (RND3) were diagnosed as the top hub genes in the up- and down-regulated PPI network and modules. In addition, GATA binding protein 6 (GATA6), ectonucleotide pyrophosphatase/phosphodiesterase 5 (ENPP5), cyclin D1 (CCND1) and tubulin, beta 2A (TUBB2A) were diagnosed as the top hub genes in the up- and down-regulated target gene–miRNA network, while tubulin, beta 2A (TUBB2A), olfactomedin-like 1 (OLFML1), prostate adrogen-regulated mucin-like protein 1 (PARM1) and aldehyde dehydrogenase 4 family, member A1 (ALDH4A1)were diagnosed as the top hub genes in the up- and down-regulated target gene–TF network. The current study based on the GEO database provides a novel understanding regarding the mechanism of insulin resistance and may provide novel therapeutic targets. Full article

(This article belongs to the Special Issue Obesity and Hormones)

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8 pages, 2549 KiB

Open AccessCommunication

Simple Analysis of Lipid Inhibition Activity on an Adipocyte Micro-Cell Pattern Chip

by Gi Yong Kim, Su-Jin Yeom, Sung-Chan Jang, Chang-Soo Lee, Changhyun Roh and Heon-Ho Jeong

Biomolecules 2018, 8(2), 37; https://doi.org/10.3390/biom8020037 - 04 Jun 2018

Cited by 8 | Viewed by 4219

Abstract

Polydimethyl-siloxane (PDMS) is often applied to fabricate cell chips. In this study, we fabricated an adipocyte microcell pattern chips using PDMS to analyze the inhibition activity of lipid droplets in mouse embryo fibroblast cells (3T3-L1) with anti-obesity agents. To form the PDMS based micropattern, we applied the micro-contact printing technique using PDMS micro-stamps that had been fabricated by conventional soft lithography. This PDMS micro-pattern enabled the selective growth of 3T3-L1 cells onto the specific region by preventing cell adhesion on the PDMS region. It then allowed growth of the 3T3-L1 cells in the chip for 10 days and confirmed that lipid droplets were formed in the 3T3-L1 cells. After treatment of orlistat and quercetin were treated in an adipocyte micro-cell pattern chip with 3T3-L1 cells for six days, we found that orlistat and quercetin exhibited fat inhibition capacities of 19.3% and 24.4% from 0.2 μM of lipid droplets in 3T3-L1 cells. In addition, we conducted a direct quantitative analysis of 3T3-L1 cell differentiation using Oil Red O staining. In conclusion, PDMS-based adipocyte micro-cell pattern chips may contribute to the development of novel bioactive compounds. Full article

(This article belongs to the Special Issue Obesity and Hormones)

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Review

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28 pages, 2341 KiB

Open AccessReview

Role of Obesity, Mesenteric Adipose Tissue, and Adipokines in Inflammatory Bowel Diseases

by Jan Bilski, Agnieszka Mazur-Bialy, Dagmara Wojcik, Marcin Surmiak, Marcin Magierowski, Zbigniew Sliwowski, Robert Pajdo, Slawomir Kwiecien, Aleksandra Danielak, Agata Ptak-Belowska and Thomas Brzozowski

Biomolecules 2019, 9(12), 780; https://doi.org/10.3390/biom9120780 - 26 Nov 2019

Cited by 67 | Viewed by 8795

Abstract

Inflammatory bowel diseases (IBDs) are a group of disorders which include ulcerative colitis and Crohn’s disease. Obesity is becoming increasingly more common among patients with inflammatory bowel disease and plays a role in the development and course of the disease. This is especially true in the case of Crohn’s disease. The recent results indicate a special role of visceral adipose tissue and particularly mesenteric adipose tissue, also known as “creeping fat”, in pathomechanism, leading to intestinal inflammation. The involvement of altered adipocyte function and the deregulated production of adipokines, such as leptin and adiponectin, has been suggested in pathogenesis of IBD. In this review, we discuss the epidemiology and pathophysiology of obesity in IBD, the influence of a Western diet on the course of Crohn’s disease and colitis in IBD patients and animal’s models, and the potential role of adipokines in these disorders. Since altered body composition, decrease of skeletal muscle mass, and development of pathologically changed mesenteric white adipose tissue are well-known features of IBD and especially of Crohn’s disease, we discuss the possible crosstalk between adipokines and myokines released from skeletal muscle during exercise with moderate or forced intensity. The emerging role of microbiota and the antioxidative and anti-inflammatory enzymes such as intestinal alkaline phosphatase is also discussed, in order to open new avenues for the therapy against intestinal perturbations associated with IBD. Full article

(This article belongs to the Special Issue Obesity and Hormones)

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