scholarly journals 5-Hydroxytryptophan (5-HTP): Natural Occurrence, Analysis, Biosynthesis, Biotechnology, Physiology and Toxicology

2020 ◽  
Vol 22 (1) ◽  
pp. 181
Author(s):  
Massimo E. Maffei
Keyword(s):  
Animal Studies ◽  
Tryptophan Hydroxylase ◽  
Metabolic Diseases ◽  
Physiological Role ◽  
Molecular Engineering ◽  
Natural Occurrence ◽  
Treatment Of Depression ◽  
Analysis And Synthesis ◽  
Natural Component

L-5-hydroxytryptophan (5-HTP) is both a drug and a natural component of some dietary supplements. 5-HTP is produced from tryptophan by tryptophan hydroxylase (TPH), which is present in two isoforms (TPH1 and TPH2). Decarboxylation of 5-HTP yields serotonin (5-hydroxytryptamine, 5-HT) that is further transformed to melatonin (N-acetyl-5-methoxytryptamine). 5-HTP plays a major role both in neurologic and metabolic diseases and its synthesis from tryptophan represents the limiting step in serotonin and melatonin biosynthesis. In this review, after an look at the main natural sources of 5-HTP, the chemical analysis and synthesis, biosynthesis and microbial production of 5-HTP by molecular engineering will be described. The physiological effects of 5-HTP are discussed in both animal studies and human clinical trials. The physiological role of 5-HTP in the treatment of depression, anxiety, panic, sleep disorders, obesity, myoclonus and serotonin syndrome are also discussed. 5-HTP toxicity and the occurrence of toxic impurities present in tryptophan and 5-HTP preparations are also discussed.

scholarly journals Glucagon Receptor Signaling and Glucagon Resistance

2019 ◽  
Vol 20 (13) ◽  
pp. 3314 ◽  
Author(s):  
Janah ◽  
Kjeldsen ◽  
Galsgaard ◽  
Winther-Sørensen ◽  
Stojanovska ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Amino Acid ◽  
Amino Acid Metabolism ◽  
Acid Metabolism ◽  
Metabolic Diseases ◽  
Physiological Role ◽  
Glucagon Receptor ◽  
Metabolomic Profiling ◽  
Hepatic Fat

Hundred years after the discovery of glucagon, its biology remains enigmatic. Accurate measurement of glucagon has been essential for uncovering its pathological hypersecretion that underlies various metabolic diseases including not only diabetes and liver diseases but also cancers (glucagonomas). The suggested key role of glucagon in the development of diabetes has been termed the bihormonal hypothesis. However, studying tissue-specific knockout of the glucagon receptor has revealed that the physiological role of glucagon may extend beyond blood-glucose regulation. Decades ago, animal and human studies reported an important role of glucagon in amino acid metabolism through ureagenesis. Using modern technologies such as metabolomic profiling, knowledge about the effects of glucagon on amino acid metabolism has been expanded and the mechanisms involved further delineated. Glucagon receptor antagonists have indirectly put focus on glucagon’s potential role in lipid metabolism, as individuals treated with these antagonists showed dyslipidemia and increased hepatic fat. One emerging field in glucagon biology now seems to include the concept of hepatic glucagon resistance. Here, we discuss the roles of glucagon in glucose homeostasis, amino acid metabolism, and lipid metabolism and present speculations on the molecular pathways causing and associating with postulated hepatic glucagon resistance.

scholarly journals Effect of 1,5-Anhydro-D-Fructose on the Inhibition of Adipogenesis in 3T3-L1 Adipocytes

2012 ◽  
Vol 7 (11) ◽  
pp. 1934578X1200701 ◽  
Author(s):  
Akiko Kojima-Yuasa ◽  
Yohei Deguchi ◽  
Yotaro Konishi ◽  
Isao Matsui-Yuasa
Keyword(s):  
Metabolic Diseases ◽  
Physiological Role ◽  
Structural Similarity ◽  
Regulation Of Transcription ◽  
Energy Sensor ◽  
Mammalian Tissues ◽  
Cellular Lipid Accumulation ◽  
Amp Activated Protein Kinase

1,5-Anhydro-D-fructose (1,5-AF) is a monosaccharide that shares a structural similarity to glucose. 1,5-AF is found in fungi, algae, Escherichia coli and rat liver and is produced by the degradation of starch and glycogen, which is catalyzed by the enzyme α-1,4-glucan lyase. However, the physiological role of 1,5-AF in mammalian tissues is not well understood. Here, we investigated the anti-obesity potential of 1,5-AF on adipogenesis in 3T3-L1 adipocytes. 1,5-AF caused a significant decrease in GPDH activity in 3T3-L1 preadipocytes and mature adipocytes without eliciting cytotoxicity, and inhibited cellular lipid accumulation through down-regulation of transcription factors such as PPARγ and C/EBPα. 1,5-AF also induced dose-dependent phosphorylation of AMP-activated protein kinase (AMPK), a cellular energy sensor. However, the total AMPK protein content remained unchanged. Furthermore, 1,5-AF increased the levels of reactive oxygen species, an important upstream signal for AMPK activation in 3T3-L1 adipocytes. Our results show that 1,5-AF exerts anti-obesity action in vitro and suggest that 1,5-AF is potentially a novel preventative agent for obesity and other metabolic diseases.

Role of Chemically Modified Tetracyclines in the Management of Periodontal Diseases: A Review

Drug Research ◽  
2017 ◽  
Vol 67 (05) ◽  
pp. 258-265 ◽  
Author(s):  
Archit Ghangurde ◽  
Kiran Ganji ◽  
Manohar Bhongade ◽  
Bhumika Sehdev
Keyword(s):  
Animal Studies ◽  
Metabolic Diseases ◽  
Periodontal Diseases ◽  
Gelatinase Activity ◽  
Chemically Modified ◽  
Periodontal Breakdown ◽  
Osteoclast Function ◽  
Chemically Modified Tetracyclines

AbstractResearchers have found that Chemically Modified Tetracyclines (CMTs) act through multiple mechanisms, affecting several parameters of osteoclast function and consequently inhibit bone resorption by altering intracellular calcium concentration and interacting with the putative calcium receptor; decreasing ruffled border area; diminishing acid production; diminishing the secretion of lysosomal cysteine proteinases (cathepsins); inducing cell retraction by affecting podosomes; inhibiting osteoclast gelatinase activity; selectively inhibiting osteoclast ontogeny or development; and inducing apoptosis or programmed cell death of osteoclasts. Thus TCs/CMTs, as anti-resorptive drugs, may act similarly to bisphosphonates and primarily affect osteoclast function. Researchers have evaluated the influence of various chemically modified tetracyclines from CMT-1 to CMT-10 on collagenases and gelatinases through in vitro or animal studies and concluded that all the CMTs except CMT-5 inhibited periodontal breakdown through MMP inhibition in the following order of efficacy: CMT-8>CMT-1>CMT-3>CMT-4>CMT-7. Thus the non-antimicrobial actions of the chemically modified analogues of tetracyclines have shown remarkably better mechanisms to those of agents with established anti-inflammatory/antioxidant potential. These findings clarify the multi-faceted actions of tetracyclines which are unique amongst antimicrobials, with therapeutic applications in periodontal and metabolic diseases. Hence, the present review describes the role of chemically modified tetracyclines in the management of periodontal diseases.

scholarly journals ANGPTL8 in metabolic homeostasis: more friend than foe?

Open Biology ◽  
2021 ◽  
Vol 11 (9) ◽  
Author(s):  
Chang Guo ◽  
Chenxi Wang ◽  
Xia Deng ◽  
Jianqiang He ◽  
Ling Yang ◽  
...  
Keyword(s):  
Metabolic Disorders ◽  
Metabolic Diseases ◽  
Hepatic Glucose Production ◽  
Physiological Role ◽  
Glucose Production ◽  
Peripheral Tissues ◽  
Glucose And Lipid Metabolism ◽  
Hepatic Glucose

ANGPTL8 is an important cytokine, which is significantly increased in type 2 diabetes mellitus (T2DM), obesity and metabolic syndrome. Many studies have shown that ANGPTL8 can be used as a bio-marker of these metabolic disorders related diseases, and the baseline ANGPTL8 level has also been found to be positively correlated with retinopathy and all-cause mortality in patients with T2DM. This may be related to the inhibition of lipoprotein lipase activity and the reduction of circulating triglyceride (TG) clearance by ANGPTL8. Consistently, inhibition of ANGPTL8 seems to prevent or improve atherosclerosis. However, it is puzzling that ANGPTL8 seems to have a directing function for TG uptake in peripheral tissues; that is, ANGPTL8 specifically enhances the reserve and buffering function of white adipose tissue, which may alleviate the ectopic lipid accumulation to a certain extent. Furthermore, ANGPTL8 can improve insulin sensitivity and inhibit hepatic glucose production. These contradictory results lead to different opinions on the role of ANGPTL8 in metabolic disorders. In this paper, the correlation between ANGPTL8 and metabolic diseases, the regulation of ANGPTL8 and the physiological role of ANGPTL8 in the process of glucose and lipid metabolism were summarized, and the physiological/pathological significance of ANGPTL8 in the process of metabolic disorder was discussed.

scholarly journals The role of gut microbiota in the effects of maternal obesity during pregnancy on offspring metabolism

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Liyuan Zhou ◽  
Xinhua Xiao
Keyword(s):  
Gut Microbiota ◽  
Animal Studies ◽  
Maternal Obesity ◽  
Metabolic Diseases ◽  
Microbial Colonization ◽  
Global Epidemic ◽  
Increased Risk ◽  
Colonization Hypothesis ◽  
The Impact

Obesity is considered a global epidemic. Specifically, obesity during pregnancy programs an increased risk of the offspring developing metabolic disorders in addition to the adverse effects on the mother per se. Large numbers of human and animal studies have demonstrated that the gut microbiota plays a pivotal role in obesity and metabolic diseases. Similarly, maternal obesity during pregnancy is associated with alterations in the composition and diversity of the intestine microbial community. Recently, the microbiota in the placenta, amniotic fluid, and meconium in healthy gestations has been investigated, and the results supported the “in utero colonization hypothesis” and challenged the traditional “sterile womb” that has been acknowledged worldwide for more than a century. Thus, the offspring microbiota, which is crucial for the immune and metabolic function and further health in the offspring, might be established prior to birth. As a detrimental intrauterine environment, maternal obesity influences the microbial colonization and increases the risk of metabolic diseases in offspring. This review discusses the role of the microbiota in the impact of maternal obesity during pregnancy on offspring metabolism and further analyzes related probiotic or prebiotic interventions to prevent and treat obesity and metabolic diseases.

The role of vitamin A and its pro-vitamin carotenoids in fetal and neonatal programming: gaps in knowledge and metabolic pathways

2020 ◽  
Vol 79 (1) ◽  
pp. 76-87
Author(s):  
Leonardo M de Souza Mesquita ◽  
Laís V Mennitti ◽  
Veridiana V de Rosso ◽  
Luciana P Pisani
Keyword(s):  
Vitamin A ◽  
Nutritional Status ◽  
Metabolic Pathways ◽  
Metabolic Diseases ◽  
Biological Effects ◽  
Physiological Role ◽  
Current Data ◽  
Cellular Processes ◽  
Pregnancy And Lactation

Abstract Vitamin A (VA) and its pro-vitamin carotenoids are naturally occurring lipophilic compounds involved in several cellular processes and metabolic pathways. Despite their broad spectrum of activities in the general population, dietary deficiencies of these compounds can potentially affect pregnancy outcomes. Since maternal nutritional status and diet composition during pregnancy and lactation can have long-lasting effects in offspring until adulthood, this study presents an overview of VA and the role of pro-VA carotenoids during pregnancy and lactation – the nutrition, metabolism, and biological effects in the offspring. The review aimed to discuss the pro-VA carotenoids and VA-associated pathways and summarize the results with reference to gestational disorders, and VA and pro-VA carotenoids as preventive agents. Also, considering that obesity, overweight, and metabolic diseases are major public health concerns worldwide, fetal and neonatal development is discussed, highlighting the physiological role of these molecules in obesity prevention. This review comprehensively summarizes the current data and shows the potential impact of these compounds on nutritional status in pregnancy and lactation.

scholarly journals Natural occurrence and physiological role of a truncated eIF4E in the porcine endometrium during implantation

2010 ◽  
Vol 432 (2) ◽  
pp. 353-363 ◽  
Author(s):  
Karin Wollenhaupt ◽  
Kati Reinke ◽  
Klaus-Peter Brüssow ◽  
Dirk Albrecht ◽  
Ute Tiemann ◽  
...  
Keyword(s):  
Binding Protein ◽  
Physiological Role ◽  
Northern Blotting ◽  
Initiation Factor ◽  
Regulation Mechanism ◽  
Natural Occurrence ◽  
Translational Initiation ◽  
Free Translation

The present study is the first report providing evidence for a physiological role of a truncated form of the mRNA cap-binding protein eIF4E1 (eukaryotic initiation factor 4E1). Our initial observation was that eIF4E, which mediates the mRNA cap function by recruiting the eIF4F complex (composed of eIF4E, 4G and 4A), occurs in two forms in porcine endometrial tissue in a strictly temporally restricted fashion. The ubiquitous prototypical 25 kDa form of eIF4E was found in ovariectomized and cyclic animals. A new stable 23 kDa variant, however, is predominant during early pregnancy at the time of implantation. Northern blotting, cDNA sequence analysis, in vitro protease assays and MS showed that the 23 kDa form does not belong to a new class of eIF4E proteins. It represents a proteolytically processed variant of eIF4E1, lacking not more than 21 amino acids at the N-terminus. Steroid replacements indicated that progesterone in combination with 17β-oestradiol induced the formation of the 23 kDa eIF4E. Modified cell-free translation systems mimicking the situation in the endometrium revealed that, besides eIF4E, eIF4G was also truncated, but not eIF4A or PABP [poly(A)-binding protein]. The 23 kDa form of eIF4E reduced the repressive function of 4E-BP1 (eIF4E-binding protein 1) and the truncated eIF4G lacked the PABP-binding site. Thus we suggest that the truncated eIF4E provides an alternative regulation mechanism by an altered dynamic of eIF4E/4E-BP1 binding under conditions where 4E-BP1 is hypophosphorylated. Together with the impaired eIF4G–PABP interaction, the modified translational initiation might particularly regulate protein synthesis during conceptus attachment at the time of implantation.

Asynchronous Generation Of Kinin And Kallikrein Activity Following Soluble Activation Of Plasma

1981 ◽  
Author(s):  
A M Bubnic ◽  
T R Zuffi ◽  
M A Fournel
Keyword(s):  
Generation Time ◽  
Animal Studies ◽  
Dextran Sulfate ◽  
Physiological Role ◽  
Factor Xii ◽  
Kallikrein Activity ◽  
Kinetics Of

In an effort to assess the physiological significance of a soluble activator of Factor XII, the kinetics of F. XII and prekallikrein activation and subsequent kinin formation have been investigated using dextran sulfate. Employing an amidolytic assay for kallikrein and a bioassay for kinin activity a reproducible lag in the generation of detectable kallikrein activity has been demonstrated in the presence of explosive kinin generation. Time, temperature and concentration kinetics have been determined as well as characterization of this system with prekallikrein activator (PKA; B-XIIa; XIIf), selective inhibitors and deficient plasmas. These studies have shown that kinin activity is generated in substantial amounts prior to the generation of any significant kallikrein activity by the activation of F. XII, suggesting that the physiological role of prekallikrein activation in kinin generation may be relatively minor. In vivo animal studies with PKA appear to confirm this finding with insignificant alterations in prekallikrein titers in the presence of marked systemic kinin-mediated hypotension.

scholarly journals Emerging Role of Mast Cells and Macrophages in Cardiovascular and Metabolic Diseases

2012 ◽  
Vol 33 (1) ◽  
pp. 71-108 ◽  
Author(s):  
Jia-Ming Xu ◽  
Guo-Ping Shi
Keyword(s):  
Mast Cells ◽  
Cell Biology ◽  
Animal Studies ◽  
Matrix Protein ◽  
Metabolic Diseases ◽  
Inflammatory Cells ◽  
Cardiovascular Complications ◽  
Over The Counter ◽  
Cell Recruitment

Mast cells are essential in allergic immune responses. Recent discoveries have revealed their direct participation in cardiovascular diseases and metabolic disorders. Although more sophisticated mechanisms are still unknown, data from animal studies suggest that mast cells act similarly to macrophages and other inflammatory cells and contribute to human diseases through cell–cell interactions and the release of proinflammatory cytokines, chemokines, and proteases to induce inflammatory cell recruitment, cell apoptosis, angiogenesis, and matrix protein remodeling. Reduced cardiovascular complications and improved metabolic symptoms in animals receiving over-the-counter antiallergy medications that stabilize mast cells open another era of mast cell biology and bring new hope to human patients suffering from these conditions.

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