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The Role of Neurotensin in Control of Anterior Pituitary Hormone Secretion
Published in Craig A. Johnston, Charles D. Barnes, Brain-Gut Peptides and Reproductive Function, 2020
While attempting to purify corticotropin-releasing factor from hypothalamic extracts, Susan Leeman noticed that the rats salivated following injection of certain fractions (Leeman and Carraway, 1982). She and her associates characterized the molecule responsible for this sialogogic activity. It was substance P (Chang and Leeman, 1970). While screening columns to locate sialogogic activity, she noticed a characteristic vasodilatation of exposed cutaneous regions, particularly around the face and ears of the assay rats. She and her associates went on to isolate and determine the structure of this vasodilatory peptide which was named neurotensin (Carraway and Leeman, 1973). The structure of the tridecapeptide (Fig. 1) has pyroglutamic acid at the N-terminal and a carboxyl group at the C-terminal end of the molecule.
Endocrine Functions of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
GnRH is a linear decapeptide with two protected termini: pyroglutamic acid at the N-terminus and carboxyamide at the C-terminus. It is a product of the GNRH1 gene, located on chromosome 8p11.2. Similar to other neuropeptides, GnRH is synthesized as part of a large prohormone that is cleaved enzymatically and is further modified within the secretory granules. Cleavage of the prohormone generates the GnRH decapeptide and a 56-amino acid GnRH-associated protein (GAP), which is secreted together with GnRH. The function of GAP is unknown but it inhibits PRL release in some species. A second human gene, named GnRH-II, was later cloned and mapped to chromosome 20p13. The most prominent difference in tissue distribution of GnRH-I and GnRH-II in humans is that expression of GnRH-I is confined to the brain, whereas GnRH-II is expressed at the highest level outside the brain, i.e., kidney, bone marrow and prostate [65].
Additional Supplements That Support Glycemic Control and Reduce Chronic Inflammation
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
A clinical study conducted in Tunisia and reported in the Journal of the American College of Nutrition aimed to determine the effects of combined zinc (Zn) and chromium (Cr) supplementation on oxidative stress and glucose homeostasis in people with Type 2 diabetes. Adults with HbA1c greater than 7.5% were supplemented for 6 months with 30 mg/day of Zn, as Zn gluconate, or 400 μg/day of Cr, as Cr pidolate (pidolate: pyroglutamic acid), or combined Zn/Cr supplementation, or placebo.
Liver metabolomic characterization of Sophora flavescens alcohol extract-induced hepatotoxicity in rats through UPLC/LTQ-Orbitrap mass spectrometry
Published in Xenobiotica, 2020
Peng Jiang, Yancai Sun, Nengneng Cheng
Glutathione is an essential cellular antioxidant synthesized from glutamine carbons. Glutathione can prevent cellular damage caused by alkylating agents and free radicals by binding to electrophilic chemicals. Glutathione, especially in the liver, binds to toxic chemicals to detoxify them. Pyroglutamic acid is a cyclized intermediate in the γ-glutamyl cycle, a pathway for glutathione biosynthesis and degradation. This intermediate is also related to redox imbalance. Increased levels of pyroglutamic acid and glutathione might reflect the hepatotoxicity of SFAE associated with the disturbance of glutathione metabolism.
Preformulation studies of l -glutathione: physicochemical properties, degradation kinetics, and in vitro cytotoxicity investigations
Published in Drug Development and Industrial Pharmacy, 2020
Mengyang Liu, Manisha Sharma, Guo-Liang Lu, Naibo Yin, Murad Al Gailani, Sree Sreebhavan, Jingyuan Wen
The unknown peaks (peak 1*, 2*, 3*, 4*, 5*, 6*, and 7*) observed in HPLC analysis of GSH degradation were identified by high resolution LC-MS. The seven mass peaks shown in Figure 11 were detected and attributed to GSSG (a: peak 1*), cysteinyl glycine (b: peak 2*), pyroglutamic acid (c: peak 3*), glutathione (d: drug main peak), glutamic acid (e: peak 4*), glutathione sulfinate (f: peak 5*), gamma-glutamylcysteine dioxide (g: peak 6*) and glutathione sulfonic acid (h: peak 7*). It was observed that in acidic conditions, the main degradation products were glutathione disulfide, cysteinyl glycine, glutathione, pyroglutamic acid, glutamic acid, and to a lesser extent GSSG. These (acidic) degradation products indicate amide bond cleavage between glutamate and cysteine, which was further acid-catalyzed into pyroglutamic acid. Under basic conditions there was also amide bond cleavage between glutamate and cysteine but also the amide bond between cysteine and glycine was cleaved to form glutamic cysteine sulfonate, which was further base-catalyzed into gamma-glutamylcysteine dioxide (peak 6*). A small amount of GSH was also oxidized into glutathione sulfinate in basic conditions. Expectedly, in the presence of pure water and artificial light only the formation of GSSG by oxidation was observed without any amide bond cleavage due to its autoxidation. Exposing GSH to high temperatures would result in amide bond breakage, but only between glutamate and cysteine. Treatment of GSH with hydrogen peroxide leads to the formation of GSSG (peak 1*) with a small amount of glutathione sulfonic acid (peak 7*). In summary, a schematic degradation scheme of GSH in different conditions is shown in Figure 12. The different degradation mechanisms and kinetics corresponded to a specific degradation kinetic model analysis (two kinetic orders existed in six different conditions).
Targeted metabolomics as a tool for the diagnosis of kidney disease in Type II diabetes mellitus
Published in British Journal of Biomedical Science, 2021
S Abdelsattar, ZA Kasemy, M Elsayed, TA Elrahem, SK Zewain
Compared with blood metabolomics, urine metabolomics may offer a straight understanding of biological pathways related to kidney dysfunction as urine metabolites are directly emitted by the kidney [35]. Organic anion transporters (OAT), which were involved in the elimination of these organic anions via the kidney, are affected in DKD. This hypothesis was supported, as there was a greater than twofold reduction in the gene expression levels of OAT1 and OAT3 in kidney biopsy samples from patients with diabetic nephropathy compared with that of the non-diseased kidney [36]. Analysis of the organic acids in the current study revealed that the tricarboxylic cycle metabolites had a significantly highly increasing linear trend over the three groups that could be an indicator of kidney function [37]. Remarkably, the main bulk of the 17 organic acids or the enzymes generating metabolites is oxidized in mitochondria, therefore implicating mitochondrial dysfunction and reduced mitochondrial biogenesis as the main feature associated with early DKD [15]. The metabolite 5-hydroxyhexanoic acid is produced from fatty acids degradation with medium-chain lengths (particularly hexanoic acid) [35]. Its level showed a highly significant decreasing trend in the groups of early DKD, this was in line with the study of Tang et al, that may increase the risk of ESRD progression in T2DM patients with microalbuminuria [35]. A novel view of this metabolism could present a probable new medical theory for the avoidance of renal function decline by increasing their levels, such as supplementation which necessitates further confirmation [35]. In addition, the diseased groups showed a highly decreasing trend of azelaic acid in urine. Azelaic acid increases the amounts of enzymatic and nonenzymatic antioxidants that was related to the development of DKD [35]. Furthermore, L-pyroglutamic acid showed an increasing trend in the diseased groups, in accordance with the study of Kim et al. [38] due to impaired fasting glucose of the diabetic subjects [38]. These results provide new pathogenetic phases that may be new targets for treatment.