E-Mail Alert

Add your e-mail address to receive forthcoming issues of this journal:

Journal Browser

Journal Browser

Special Issue "Marine Drugs in the Management of Metabolic Diseases"

A special issue of Marine Drugs (ISSN 1660-3397).

Deadline for manuscript submissions: 30 June 2018

Special Issue Editor

Guest Editor
Dr. Graciliana Lopes

REQUIMTE/LAQV, Laboratório de Farmacognosia, Departamento de Química, Faculdade de Farmácia, Universidade do Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal
E-Mail
Interests: marine drugs; drug discovery; Diabetes mellitus; oxidative stress; seaweed bioactive compounds; phlorotannins

Special Issue Information

Dear Colleagues,

Metabolic diseases consist of complex heterogeneous disorders caused by the breakdown of body homeostasis, which greatly affect individuals’ quality of life. Mainly due to significant changes in human lifestyle, such as sedentarism, excess calories and exponential growth of emotional stress, metabolic diseases have been the current target of public health and scientific concern.

Marine organisms are rich sources of bioactive compounds with diverse molecular structures and biological activities, which place them at the forefront as the most appealing sources of drug leads in the 21st century. In addition to constituting privileged targets of chemical and molecular studies, marine drugs have a privileged role in pharmaceutical bioprospecting, representing a new hope for the management of metabolic diseases.

In this Special Issue, we are seeking original and high quality research articles, as well as reviews, focused on marine drugs with potential for the pharmacological management of metabolic diseases, with emphasis on diabetes mellitus, dyslipidaemia and gut. We intend to highlight surveys concerning novel compounds from marine sources, with relevant prospects on metabolic diseases related processes.

Dr. Graciliana Lopes
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Marine Drugs is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Metabolic diseases (Diabetes mellitus, Gut, Dyslipidaemia, Hypertension)
  • Mechanism of action
  • Compounds isolation and molecular modulation
  • Genetic modulation of mediators involved in metabolism homeostasis
  • Structure-activity relationship

Published Papers (5 papers)

View options order results:
result details:
Displaying articles 1-5
Export citation of selected articles as:

Research

Open AccessArticle Chitin Oligosaccharide Modulates Gut Microbiota and Attenuates High-Fat-Diet-Induced Metabolic Syndrome in Mice
Mar. Drugs 2018, 16(2), 66; doi:10.3390/md16020066
Received: 22 January 2018 / Revised: 10 February 2018 / Accepted: 17 February 2018 / Published: 19 February 2018
PDF Full-text (4415 KB) | HTML Full-text | XML Full-text
Abstract
Gut microbiota has been proved to be an indispensable link between nutrient excess and metabolic syndrome, and chitin oligosaccharide (NACOS) has displayed therapeutic effects on multiple diseases such as cancer and gastritis. In this study, we aim to confirm whether NACOS can ameliorate
[...] Read more.
Gut microbiota has been proved to be an indispensable link between nutrient excess and metabolic syndrome, and chitin oligosaccharide (NACOS) has displayed therapeutic effects on multiple diseases such as cancer and gastritis. In this study, we aim to confirm whether NACOS can ameliorate high-fat diet (HFD)-induced metabolic syndrome by rebuilding the structure of the gut microbiota community. Male C57BL/6J mice fed with HFD were treated with NACOS (1 mg/mL) in drinking water for five months. The results indicate that NACOS improved glucose metabolic disorder in HFD-fed mice and suppressed mRNA expression of the protein regulators related to lipogenesis, gluconeogenesis, adipocyte differentiation, and inflammation in adipose tissues. Additionally, NACOS inhibited the destruction of the gut barrier in HFD-treated mice. Furthermore, 16S ribosome RNA sequencing of fecal samples demonstrates that NACOS promoted the growth of beneficial intestinal bacteria remarkably and decreased the abundance of inflammogenic taxa. In summary, NACOS partly rebuilt the microbial community and improved the metabolic syndrome of HFD-fed mice. These data confirm the preventive effects of NACOS on nutrient excess-related metabolic diseases. Full article
(This article belongs to the Special Issue Marine Drugs in the Management of Metabolic Diseases)
Figures

Figure 1

Open AccessArticle Combination Treatment of Deep Sea Water and Fucoidan Attenuates High Glucose-Induced Insulin-Resistance in HepG2 Hepatocytes
Mar. Drugs 2018, 16(2), 48; doi:10.3390/md16020048
Received: 26 November 2017 / Revised: 26 January 2018 / Accepted: 31 January 2018 / Published: 2 February 2018
PDF Full-text (1681 KB) | HTML Full-text | XML Full-text
Abstract
Insulin resistance (IR) plays a central role in the development of several metabolic diseases, which leads to increased morbidity and mortality rates, in addition to soaring health-care costs. Deep sea water (DSW) and fucoidans (FPS) have drawn much attention in recent years because
[...] Read more.
Insulin resistance (IR) plays a central role in the development of several metabolic diseases, which leads to increased morbidity and mortality rates, in addition to soaring health-care costs. Deep sea water (DSW) and fucoidans (FPS) have drawn much attention in recent years because of their potential medical and pharmaceutical applications. This study investigated the effects and mechanisms of combination treatment of DSW and FPS in improving IR in HepG2 hepatocytes induced by a high glucose concentration. The results elucidated that co-treatment with DSW and FPS could synergistically repress hepatic glucose production and increase the glycogen level in IR-HepG2 cells. In addition, they stimulated the phosphorylation levels of the components of the insulin signaling pathway, including tyrosine phosphorylation of IRS-1, and serine phosphorylation of Akt and GSK-3β. Furthermore, they increased the phosphorylation of AMPK and ACC, which in turn decreased the intracellular triglyceride level. Taken together, these results suggested that co-treatment with DSW and FPS had a greater improving effect than DSW or FPS alone on IR. They might attenuate IR by targeting Akt/GSK-3β and AMPK pathways. These results may have some implications in the treatment of metabolic diseases. Full article
(This article belongs to the Special Issue Marine Drugs in the Management of Metabolic Diseases)
Figures

Open AccessArticle Protective Effect of Meretrix meretrix Oligopeptides on High-Fat-Diet-Induced Non-Alcoholic Fatty Liver Disease in Mice
Mar. Drugs 2018, 16(2), 39; doi:10.3390/md16020039
Received: 11 December 2017 / Revised: 9 January 2018 / Accepted: 20 January 2018 / Published: 23 January 2018
PDF Full-text (7185 KB) | HTML Full-text | XML Full-text
Abstract
The present study investigated the effects of MMO (Meretrix meretrix oligopeptides) on mice fed a high-fat diet. Mice were fed either a normal control diet (NC) or a high-fat diet (HFD) without or with MMO (50 mg/kg or 250 mg/kg) for four
[...] Read more.
The present study investigated the effects of MMO (Meretrix meretrix oligopeptides) on mice fed a high-fat diet. Mice were fed either a normal control diet (NC) or a high-fat diet (HFD) without or with MMO (50 mg/kg or 250 mg/kg) for four weeks. Levels of ALT, AST, liver tissue GSH-Px, and SOD activities, MDA levels were measured using commercially available kits; HE staining was performed to analyze pathologic changes of the liver; a TEM assay was performed to measure the ultrastructural alterations of the mitochondria, and Western blotting was performed to detect the expression of gene proteins related to lipid metabolism, inflammation, and liver apoptosis. After six weeks, body weight, ALT, AST, and MDA levels were significantly increased, and GSH-Px levels and SOD activities were significantly decreased in the HFD control group compared with the NC group. Consumption of the HFD compared with the NC caused fatty liver abnormal mitochondria with loss of cristae, intramitochondrial granules, and a swollen and rarefied matrix. Administration of MMO significantly decreased body weight gain, and ALT, AST, and MDA levels; increased SOD activity and GSH-Px levels; alleviated fatty liver steatosis; decreased the early apoptosis population; downregulated SREBP-1c, Bax, Caspase-9, Caspase-3, TNF-α, and NF-κB protein levels; and upregulated PPAR-α, Bcl-2, and AMPK-α, compared with the HFD control group. MMO exhibited protective effects in mice with NAFLD by regulating the NF-κB anti-inflammation signaling pathways to inhibit inflammation, regulate AMPK-α, PPAR-α and SREBP-1c to improve lipid metabolism disorder, and regulate Bcl-2/Bax anti-apoptosis signaling pathways to prevent liver cell apoptosis. These results suggest that dietary supplementation with MMO ameliorates high-fat-diet-induced NAFLD. Full article
(This article belongs to the Special Issue Marine Drugs in the Management of Metabolic Diseases)
Figures

Figure 1

Open AccessArticle Lipid-Lowering Polyketides from the Fungus Penicillium Steckii HDN13-279
Mar. Drugs 2018, 16(1), 25; doi:10.3390/md16010025
Received: 2 November 2017 / Revised: 2 December 2017 / Accepted: 8 January 2018 / Published: 12 January 2018
PDF Full-text (2207 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Seven new polyketides, named tanzawaic acids R–X (16, 11), along with seven known analogues (710 and 1214), were isolated from Penicillium steckii HDN13-279. Their structures, including the absolute configurations, were elucidated by
[...] Read more.
Seven new polyketides, named tanzawaic acids R–X (16, 11), along with seven known analogues (710 and 1214), were isolated from Penicillium steckii HDN13-279. Their structures, including the absolute configurations, were elucidated by NMR, MS, X-ray diffraction, circular dichroism (CD) analyses and chemical derivatization. Five compounds (2, 3, 6, 10 and 12) significantly decreased the oleic acid (OA)-elicited lipid accumulation in HepG2 liver cells at the concentration of 10 μM, among which, four compounds (3, 6, 10 and 12) significantly decreased intracellular total cholesterol (TC) levels and three Compounds (3, 6, and 10) significantly decreased intracellular triglyceride (TG) levels. Moreover, the TG-lowering capacities of compounds 6 and 10 were comparable with those of simvastatin, with the TG levels being nearly equal to blank control. This is the first report on the lipid-lowering activity of tanzawaic acid derivatives. Full article
(This article belongs to the Special Issue Marine Drugs in the Management of Metabolic Diseases)
Figures

Open AccessArticle Deep Sea Water Improves Abnormalities in Lipid Metabolism through Lipolysis and Fatty Acid Oxidation in High-Fat Diet-Induced Obese Rats
Mar. Drugs 2017, 15(12), 386; doi:10.3390/md15120386
Received: 30 October 2017 / Revised: 29 November 2017 / Accepted: 5 December 2017 / Published: 11 December 2017
PDF Full-text (3022 KB) | HTML Full-text | XML Full-text
Abstract
Deep sea water (DSW) is a natural marine resource that has been utilized for food, agriculture, cosmetics, and medicine. The aim of this study was to investigate whether DSW has beneficial lipid metabolic effects in an animal model. Our previous in vitro study
[...] Read more.
Deep sea water (DSW) is a natural marine resource that has been utilized for food, agriculture, cosmetics, and medicine. The aim of this study was to investigate whether DSW has beneficial lipid metabolic effects in an animal model. Our previous in vitro study indicated that DSW significantly decreased the intracellular triglyceride and glycerol-3-phosphate dehydrogenase activity in 3T3-L1 adipocytes. DSW also inhibited the gene levels of adipocyte differentiation, lipogenesis, and adipocytokines, and up-regulated gene levels of lipolysis and fatty acid oxidation. In the present study, the results showed that body weight, liver, adipose tissue, hepatic triglycerides and cholesterol, and serum parameters in the high-fat diet (HFD) + DSW groups were significantly lower compared to the HFD group. Moreover, the fecal output of total lipids, triglycerides, and cholesterol in the HFD + DSW groups was significantly higher than that of the HFD group. Regarding gene expression, DSW significantly increased the gene levels of lipolysis and fatty acid oxidation, and decreased the gene levels of adipocytokine in the adipose tissue of rats with HFD-induced obesity. These results indicate a potential molecular mechanism by which DSW can suppress obesity in rats with HFD-induced obesity through lipolysis and fatty acid oxidation. Full article
(This article belongs to the Special Issue Marine Drugs in the Management of Metabolic Diseases)
Figures

Figure 1a

Back to Top