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Dimerization of hub protein DYNLL1 and bZIP transcription factor CREB3L1 enhances transcriptional activation of CREB3L1 target genes like arginine vasopressin 枢纽蛋白 DYNLL1 和 bZIP 转录因子 CREB3L1 的二聚化增强了 CREB3L1 靶基因(如精氨酸加压素)的转录激活。
IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-07-02 DOI: 10.1016/j.peptides.2024.171269
Mingkwan Greenwood, Benjamin T. Gillard, David Murphy, Michael P. Greenwood

bZIP transcription factors can function as homodimers or heterodimers through interactions with their disordered coiled-coil domain. Such dimer assemblies are known to influence DNA-binding specificity and/or the recruitment of binding partners, which can cause a functional switch of a transcription factor from being an activator to a repressor. We recently identified the genomic targets of a bZIP transcription factor called CREB3L1 in rat hypothalamic supraoptic nucleus by ChIP-seq. The objective of this study was to investigate the CREB3L1 protein-to-protein interactome of which little is known. For this approach, we created and screened a rat supraoptic nucleus yeast two-hybrid prey library with the bZIP region of rat CREB3L1 as the bait. Our yeast two-hybrid approach captured five putative CREB3L1 interacting prey proteins in the supraoptic nucleus. One interactor was selected by bioinformatic analyses for more detailed investigation by co-immunoprecipitation, immunofluorescent cellular localisation, and reporter assays in vitro. Here we identify dimerisation hub protein Dynein Light Chain LC8-Type 1 as a CREB3L1 interacting protein that in vitro enhances CREB3L1 activation of target genes.

bZIP 转录因子可通过与其无序的盘卷结构域相互作用,以同二聚体或异二聚体的形式发挥作用。众所周知,这种二聚体组装会影响 DNA 结合的特异性和/或结合伙伴的招募,从而导致转录因子从激活因子到抑制因子的功能转换。最近,我们通过 ChIP-seq 鉴定了大鼠下丘脑视上核中名为 CREB3L1 的 bZIP 转录因子的基因组靶标。本研究的目的是研究CREB3L1蛋白与蛋白之间的相互作用组,目前对其了解甚少。为此,我们创建并筛选了以大鼠 CREB3L1 的 bZIP 区为诱饵的大鼠视上核酵母双杂交猎物文库。我们的酵母双杂交方法捕获了视上核中五个可能与 CREB3L1 相互作用的猎物蛋白。通过生物信息学分析,我们选出了一个相互作用因子,并通过免疫共沉淀、免疫荧光细胞定位和体外报告实验进行了更详细的研究。在这里,我们发现二聚化枢纽蛋白Dynein Light Chain LC8-Type 1是一种CREB3L1相互作用蛋白,它在体外可增强CREB3L1对靶基因的激活。
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引用次数: 0
Endogenous opiates and behavior: 2023 内源性阿片剂与行为:2023 年。
IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-28 DOI: 10.1016/j.peptides.2024.171268
Richard J. Bodnar

This paper is the forty-sixth consecutive installment of the annual anthological review of research concerning the endogenous opioid system, summarizing articles published during 2023 that studied the behavioral effects of molecular, pharmacological and genetic manipulation of opioid peptides and receptors as well as effects of opioid/opiate agonists and antagonists. The review is subdivided into the following specific topics: molecular-biochemical effects and neurochemical localization studies of endogenous opioids and their receptors (1), the roles of these opioid peptides and receptors in pain and analgesia in animals (2) and humans (3), opioid-sensitive and opioid-insensitive effects of nonopioid analgesics (4), opioid peptide and receptor involvement in tolerance and dependence (5), stress and social status (6), learning and memory (7), eating and drinking (8), drug and alcohol abuse (9), sexual activity and hormones, pregnancy, development and endocrinology (10), mental illness and mood (11), seizures and neurologic disorders (12), electrical-related activity and neurophysiology (13), general activity and locomotion (14), gastrointestinal, renal and hepatic functions (15), cardiovascular responses (16), respiration and thermoregulation (17), and immunological responses (18).

本文是连续第四十六期有关内源性阿片系统研究的年度文选综述,总结了2023年期间发表的研究阿片肽和受体的分子、药理和遗传操作的行为效应以及阿片/阿片激动剂和拮抗剂效应的文章。综述细分为以下具体主题:内源性阿片及其受体的分子生化效应和神经化学定位研究(1),这些阿片肽和受体在动物(2)和人类(3)疼痛和镇痛中的作用,非阿片类镇痛药对阿片敏感和对阿片不敏感的效应(4),阿片肽和受体在耐受性和依赖性(5)、压力和社会地位(6)、学习和记忆(7)、饮食(8)中的参与、药物和酒精滥用(9)、性活动和荷尔蒙、妊娠、发育和内分泌(10)、精神疾病和情绪(11)、癫痫发作和神经系统疾病(12)、电相关活动和神经生理学(13)、一般活动和运动(14)、胃肠道、肾脏和肝脏功能(15)、心血管反应(16)、呼吸和体温调节(17)以及免疫反应(18)。
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引用次数: 0
Effects of hypernatremia on the microglia 高钠血症对小胶质细胞的影响
IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-20 DOI: 10.1016/j.peptides.2024.171267
Sachiho Fuse , Haruki Fujisawa , Naoya Murao , Naoko Iwata , Takashi Watanabe , Yusuke Seino , Hideyuki Takeuchi , Atsushi Suzuki , Yoshihisa Sugimura

Signs and symptoms of hypernatremia largely indicate central nervous system dysfunction. Acute hypernatremia can cause demyelinating lesions similar to that observed in osmotic demyelination syndrome (ODS). We have previously demonstrated that microglia accumulate in ODS lesions and minocycline protects against ODS by inhibiting microglial activation. However, the direct effect of rapid rise in the sodium concentrations on microglia is largely unknown. In addition, the effect of chronic hypernatremia on microglia also remains elusive. Here, we investigated the effects of acute (6 or 24 h) and chronic (the extracellular sodium concentration was increased gradually for at least 7 days) high sodium concentrations on microglia using the microglial cell line, BV-2. We found that both acute and chronic high sodium concentrations increase NOS2 expression and nitric oxide (NO) production. We also demonstrated that the expression of nuclear factor of activated T-cells-5 (NFAT5) is increased by high sodium concentrations. Furthermore, NFAT5 knockdown suppressed NOS2 expression and NO production. We also demonstrated that high sodium concentrations decreased intracellular Ca2+ concentration and an inhibitor of Na+/Ca2+ exchanger, NCX, suppressed a decrease in intracellular Ca2+ concentrations and NOS2 expression and NO production induced by high sodium concentrations. Furthermore, minocycline inhibited NOS2 expression and NO production induced by high sodium concentrations. These in vitro data suggest that microglial activity in response to high sodium concentrations is regulated by NFAT5 and Ca2+ efflux through NCX and is suppressed by minocycline.

高钠血症的体征和症状在很大程度上表明中枢神经系统功能失调。急性高钠血症可导致脱髓鞘病变,与渗透性脱髓鞘综合征(ODS)中观察到的病变相似。我们以前曾证实,小胶质细胞在 ODS 病变中聚集,而米诺环素可通过抑制小胶质细胞的活化来防止 ODS。然而,钠浓度快速升高对小胶质细胞的直接影响尚不清楚。此外,慢性高钠血症对小胶质细胞的影响也仍然难以捉摸。在这里,我们利用小胶质细胞株 BV-2 研究了急性(6 或 24 小时)和慢性(细胞外钠浓度逐渐增加至少 7 天)高钠浓度对小胶质细胞的影响。我们发现,急性和慢性高钠浓度都会增加 NOS2 的表达和一氧化氮(NO)的产生。我们还证明,高浓度钠会增加活化 T 细胞核因子-5(NFAT5)的表达。此外,NFAT5 基因敲除抑制了 NOS2 的表达和一氧化氮的产生。我们还证实,高浓度钠会降低细胞内 Ca2+ 浓度,而 Na+/Ca2+ 交换抑制剂 NCX 可抑制高浓度钠引起的细胞内 Ca2+ 浓度降低、NOS2 表达和 NO 生成。此外,米诺环素还能抑制高浓度钠诱导的 NOS2 表达和 NO 生成。这些体外数据表明,小胶质细胞对高浓度钠的反应活动受 NFAT5 和通过 NCX 的 Ca2+ 外流调节,并受米诺环素的抑制。
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引用次数: 0
Pain modulation by oxytocin 催产素对疼痛的调节
IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-17 DOI: 10.1016/j.peptides.2024.171263
Makoto Kawasaki , Akinori Sakai , Yoichi Ueta

Oxytocin (OXT) was discovered in 1906 as a substance that promotes the pregnancy and childbirth. It affects uterine contraction and lactation. Furthermore, as one of its physiological properties, it exerts analgesic effects. The living body has an ascending pathway that transmits pain stimuli from the periphery to the center and a descending pathway that regulates the dorsal horn neurons from the upper center downward. OXT is involved in the pain-inhibitory descending pathway and generally assumed to exert analgesic effects. In this article, we describe the pain-suppressive effects of OXT, among its many physiological effects.

催产素(OXT)于 1906 年被发现,是一种促进怀孕和分娩的物质。它影响子宫收缩和泌乳。此外,催产素的生理特性之一是具有镇痛作用。生物体内有一条从外周向中枢传递疼痛刺激的上升通路和一条从中枢上部向下调节背角神经元的下降通路。OXT 参与抑制疼痛的下降通路,通常被认为具有镇痛作用。在本文中,我们将介绍 OXT 在众多生理作用中的镇痛作用。
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引用次数: 0
Editorial: The rise and rise of peptide therapeutics for obesity-diabetes 社论:肥胖-糖尿病多肽疗法的兴起与发展。
IF 3 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-12 DOI: 10.1016/j.peptides.2024.171264
Peter R. Flatt, J. Michael Conlon
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引用次数: 0
Harnessing the melanocortin system in the control of food intake and glucose homeostasis 利用黑色皮质素系统控制食物摄入和葡萄糖稳态
IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-02 DOI: 10.1016/j.peptides.2024.171255
Patrick Swan , Brett Johnson , Carel W. le Roux , Alexander D. Miras

The central and peripheral melanocortin system, comprising of five receptors and their endogenous ligands, is responsible for a wide array of physiological functions such as skin pigmentation, sexual function and development, and inflammation. A growing body of both clinical and pre-clinical research is demonstrating the relevance of this system in metabolic health. Disruption of hypothalamic melanocortin signalling is the most common cause of monogenic obesity in humans. Setmelanotide, an FDA-approved analogue of alpha-melanocyte stimulating hormone (α-MSH) that functions by restoring central melanocortin signalling, has proven to be a potent pharmacological tool in the treatment of syndromic obesity. As the first effective therapy targeting the melanocortin system to treat metabolic disorders, its approval has sparked research to further harness the links between these melanocortin receptors and metabolic processes. Here, we outline the structure of the central and peripheral melanocortin system, discuss its critical role in the regulation of food intake, and review promising targets that may hold potential to treat metabolic disorders in humans.

中枢和外周黑皮质素系统由五种受体及其内源性配体组成,负责多种生理功能,如皮肤色素沉着、性功能和发育以及炎症。越来越多的临床和临床前研究表明,该系统与代谢健康息息相关。下丘脑黑皮质素信号的中断是导致人类单基因肥胖症的最常见原因。塞美拉诺肽是美国食品及药物管理局(FDA)批准的α-促黑素细胞激素(α-MSH)类似物,可通过恢复中枢黑皮质素信号发挥功能。作为第一种针对黑色素皮质素系统治疗代谢紊乱的有效疗法,它的批准引发了进一步利用这些黑色素皮质素受体与代谢过程之间联系的研究。在这里,我们将概述中枢和外周黑色素皮质素系统的结构,讨论它在调节食物摄入量中的关键作用,并回顾可能有望治疗人类代谢紊乱的靶点。
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引用次数: 0
NPYR modulation: Potential for the next major advance in obesity and type 2 diabetes management? NPYR 调节:肥胖症和 2 型糖尿病治疗的下一个重大进展的潜力?
IF 3 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-31 DOI: 10.1016/j.peptides.2024.171256
Ryan A. Lafferty, Peter R. Flatt, Nigel Irwin

The approval of the glucagon-like peptide 1 (GLP-1) mimetics semaglutide and liraglutide for management of obesity, independent of type 2 diabetes (T2DM), has initiated a resurgence of interest in gut-hormone derived peptide therapies for the management of metabolic diseases, but side-effect profile is a concern for these medicines. However, the recent approval of tirzepatide for obesity and T2DM, a glucose-dependent insulinotropic polypeptide (GIP), GLP-1 receptor co-agonist peptide therapy, may provide a somewhat more tolerable option. Despite this, an increasing number of non-incretin alternative peptides are in development for obesity, and it stands to reason that other hormones will take to the limelight in the coming years, such as peptides from the neuropeptide Y family. This narrative review outlines the therapeutic promise of the neuropeptide Y family of peptides, comprising of the 36 amino acid polypeptides neuropeptide Y (NPY), peptide tyrosine-tyrosine (PYY) and pancreatic polypeptide (PP), as well as their derivatives. This family of peptides exerts a number of metabolically relevant effects such as appetite regulation and can influence pancreatic beta-cell survival. Although some of these actions still require full translation to the human setting, potential therapeutic application in obesity and type 2 diabetes is conceivable. However, like GLP-1 and GIP, the endogenous NPY, PYY and PP peptide forms are subject to rapid in vivo degradation and inactivation by the serine peptidase, dipeptidyl-peptidase 4 (DPP-4), and hence require structural modification to prolong circulating half-life. Numerous protective modification strategies are discussed in this regard herein, alongside related impact on biological activity profile and therapeutic promise.

胰高血糖素样肽 1(GLP-1)仿制药 semaglutide 和 liraglutide 被批准用于治疗肥胖症(不包括 2 型糖尿病 (T2DM)),这再次激发了人们对肠道激素衍生肽疗法治疗代谢性疾病的兴趣,但这些药物的副作用是一个令人担忧的问题。不过,最近批准用于治疗肥胖症和 T2DM 的替扎帕肽(一种葡萄糖依赖性促胰岛素多肽 (GIP)、GLP-1 受体共拮抗剂肽类疗法)可能提供了一种更容易耐受的选择。尽管如此,越来越多治疗肥胖症的非促胰岛素替代肽正在研发中,其他激素在未来几年也将成为焦点,如神经肽 Y 家族的肽类。本综述概述了神经肽 Y 家族多肽的治疗前景,包括 36 个氨基酸的多肽神经肽 Y(NPY)、肽酪氨酸-酪氨酸(PYY)和胰多肽(PP)及其衍生物。这一系列肽具有许多与新陈代谢相关的作用,如调节食欲,并能影响胰腺β细胞的存活。虽然其中一些作用仍需要完全转化到人体环境中,但在肥胖症和 2 型糖尿病方面的潜在治疗应用是可以想象的。然而,与 GLP-1 和 GIP 一样,内源性 NPY、PYY 和 PP 肽形式在体内会被丝氨酸肽酶、二肽基肽酶 4(DPP-4)快速降解和灭活,因此需要进行结构修饰以延长循环半衰期。本文就此讨论了许多保护性修饰策略,以及对生物活性概况和治疗前景的相关影响。
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引用次数: 0
Expression patterns and behavioral effects of conopressin and APGWamide in the nudibranch Berghia stephanieae 锥体加压素和 APGWamide 在裸鳃蛙中的表达模式和行为效应。
IF 3 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-29 DOI: 10.1016/j.peptides.2024.171253
Cheyenne C. Tait , Meagan N. Olson , Kristina Nedeljkovic , Emily Kirchner , Paul S. Katz

The highly conserved oxytocin/vasopressin family of nonapeptides plays many roles across the animal kingdom, from osmoregulation to reproductive physiology. We investigated the expression patterns and pharmacological effects of the gastropod ortholog of this peptide, conopressin, along with another peptide involved in gastropod reproduction, APGWamide, in the nudibranch Berghia stephanieae. A brain transcriptome was used to identify and annotate the gene sequences for the peptides and one conopressin receptor. In-situ hybridization chain reaction showed that many neurons in the brain expressed these peptides. However, the peptide genes were co-expressed by only three neurons, which were in the right cerebral ganglion, the same side on which the reproductive organs are located. A conopressin receptor (BSCPR1) was expressed in a prominent population of APGWamide expressing neurons. Placing animals in a solution containing the APGWamide peptide caused minimal behavioral changes. However, exposure to conopressin reduced locomotion, increased gut contractions, and caused voiding at high concentration. The genes for these peptides and BSCPR1 were expressed in cells in the digestive system. BSCPR1 was also expressed by a line of neurons on the anterior portion of the radula and would be contacted during feeding. APGWamide-expressing neurons were found in the genital ganglion. All three genes expressed in cells on sensory appendages. These results are consistent with the conopressin playing a variety of roles in the brain and the body and being involved in both reproduction and digestion. This study sheds light on the function of this ancient nonapeptide in a new-to-neuroscience invertebrate species.

高度保守的催产素/血管加压素非肽家族在整个动物界扮演着从渗透调节到生殖生理的多种角色。我们研究了该肽的腹足类直向同源物--加压素以及另一种参与腹足类繁殖的肽--APGWamide在裸鳃蛙Berghia stephanieae中的表达模式和药理作用。利用脑转录组确定并注释了肽和一种加压素受体的基因序列。原位杂交连锁反应显示,大脑中的许多神经元都表达了这些肽。然而,只有三个神经元共同表达了多肽基因,它们位于右侧大脑神经节,也就是生殖器官所在的同一侧。在表达 APGWamide 的神经元群中,有一种 conopressin 受体(BSCPR1)得到了表达。将动物置于含有 APGWamide 肽的溶液中,其行为变化极小。然而,接触 conopressin 会减少运动,增加肠道收缩,并在高浓度时引起排尿。这些肽和 BSCPR1 的基因在消化系统细胞中表达。BSCPR1也在桡骨前部的一系神经元中表达,并会在进食时接触到。在生殖节中发现了表达 APGWamide 的神经元。所有三个基因都在感觉附属器上的细胞中表达。这些结果表明, conopressin 在大脑和身体中发挥着多种作用,并参与生殖和消化。这项研究揭示了这种古老的非肽类物质在神经科学新发现的无脊椎动物物种中的功能。
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引用次数: 0
Interaction of Angiotensin-(1−7) with kinins in the kidney circulation: Role of B1 receptors 肾循环中血管紧张素-(1-7)与激肽的σ相互作用:B1 受体的作用。
IF 3 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-29 DOI: 10.1016/j.peptides.2024.171246
Elizabeth Pereira Mendes , Danielle Ianzer , Diogo Barros Peruchetti , Robson Augusto Souza Santos , Maria Aparecida Ribeiro Vieira

Changes in renal hemodynamics impact renal function during physiological and pathological conditions. In this context, renal vascular resistance (RVR) is regulated by components of the Renin-Angiotensin System (RAS) and the Kallikrein-Kinin System (KKS). However, the interaction between these vasoactive peptides on RVR is still poorly understood. Here, we studied the crosstalk between angiotensin-(1−7) and kinins on RVR. The right kidneys of Wistar rats were isolated and perfused in a closed-circuit system. The perfusion pressure and renal perfusate flow were continuously monitored. Ang-(1−7) (1.0–25.0 nM) caused a sustained, dose-dependent reduction of relative RVR (rRVR). This phenomenon was sensitive to 10 nM A-779, a specific Mas receptor (MasR) antagonist. Bradykinin (BK) promoted a sustained and transient reduction in rRVR at 1.25 nM and 125 nM, respectively. The transient effect was abolished by 4 μM des-Arg9-Leu8-bradykinin (DALBK), a specific kinin B1 receptor (B1R) antagonist. Accordingly, des-Arg9-bradykinin (DABK) 1 μM (a B1R agonist) increased rRVR. Interestingly, pre-perfusion of Ang-(1−7) changed the sustained reduction of rRVR triggered by 1.25 nM BK into a transient effect. On the other hand, pre-perfusion of Ang-(1−7) primed and potentiated the DABK response, this mechanism being sensitive to A-779 and DALBK. Binding studies performed with CHO cells stably transfected with MasR, B1R, and kinin B2 receptor (B2R) showed no direct interaction between Ang-(1−7) with B1R or B2R. In conclusion, our findings suggest that Ang-(1−7) differentially modulates kinin's effect on RVR in isolated rat kidneys. These results help to expand the current knowledge regarding the crosstalk between the RAS and KKS complex network in RVR.

在生理和病理条件下,肾血流动力学的变化会影响肾功能。在这种情况下,肾血管阻力(RVR)受肾素-血管紧张素系统(RAS)和Kallikrein-激肽系统(KKS)成分的调节。然而,人们对这些血管活性肽与 RVR 之间的相互作用仍然知之甚少。在此,我们研究了血管紧张素-(1-7)和激肽对 RVR 的相互影响。我们分离了 Wistar 大鼠的右肾,并在闭路系统中进行灌注。对灌注压力和肾灌注液流量进行连续监测。Ang-(1-7)(1.0-25.0nM)导致相对 RVR(rRVR)持续、剂量依赖性降低。这种现象对 10nM A-779 很敏感,A-779 是一种特异性 Mas 受体(MasR)拮抗剂。缓激肽(BK)分别在 1.25nM 和 125nM 时促进 rRVR 的持续和短暂降低。4μM des-Arg9-Leu8-缓激肽(DALBK)(一种特异性激肽 B1 受体(B1R)拮抗剂)可消除瞬时效应。相应地,1μM des-Arg9-缓激肽(DABK)(一种 B1R 激动剂)可增加 rRVR。有趣的是,预灌注 Ang-(1-7) 使 1.25nM BK 引发的 rRVR 持续降低转变为短暂效应。另一方面,Ang-(1-7)的预灌注启动并增强了 DABK 反应,这种机制对 A-779 和 DALBK 敏感。用稳定转染 MasR、B1R 和缓激肽 B2 受体的 CHO 细胞进行的结合研究表明,Ang-(1-7)与 B1R 或 B2R 之间没有直接相互作用。总之,我们的研究结果表明,在离体大鼠肾脏中,Ang-(1-7)可不同程度地调节激肽对 RVR 的影响。这些结果有助于扩展目前有关 RAS 和 KKS 复合物网络在 RVR 中相互影响的知识。
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引用次数: 0
Chronic exposure to incretin metabolites GLP-1(9−36) and GIP(3−42) affect islet morphology and beta cell health in high fat fed mice 长期暴露于增量素代谢物 GLP-1(9-36)和 GIP(3-42)会影响高脂喂养小鼠的胰岛形态和β细胞健康。
IF 3 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-28 DOI: 10.1016/j.peptides.2024.171254
Ananyaa Sridhar, Dawood Khan, Gayathri Babu, Nigel Irwin, Victor A. Gault, Peter R. Flatt, Charlotte R. Moffett

The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are rapidly degraded by dipeptidyl peptidase-4 (DPP-4) to their major circulating metabolites GLP-1(9−36) and GIP(3−42). This study investigates the possible effects of these metabolites, and the equivalent exendin molecule Ex(9−39), on pancreatic islet morphology and constituent alpha and beta cells in high-fat diet (HFD) fed mice. Male Swiss TO-mice (6–8 weeks-old) were maintained on a HFD or normal diet (ND) for 4 months and then received twice-daily subcutaneous injections of GLP-1(9−36), GIP(3−42), Ex(9−39) (25 nmol/kg bw) or saline vehicle (0.9% (w/v) NaCl) over a 60-day period. Metabolic parameters were monitored and excised pancreatic tissues were used for immunohistochemical analysis. Body weight and assessed metabolic indices were not changed by peptide administration. GLP-1(9−36) significantly (p<0.001) increased islet density per mm2 tissue, that was decreased (p<0.05) by HFD. Islet, beta and alpha cell areas were increased (p<0.01) following HFD and subsequently reduced (p<0.01-p<0.001) by GIP(3−42) and Ex(9−39) treatment. While GLP-1(9−36) did not affect islet and beta cell areas in HFD mice, it significantly (p<0.01) decreased alpha cell area. Compared to ND and HFD mice, GIP(3−42) treatment significantly (p<0.05) increased beta cell proliferation. Whilst HFD increased (p<0.001) beta cell apoptosis, this was reduced (p<0.01-p<0.001) by both GLP-1(9−36) and GIP(3−42). These data indicate that the major circulating forms of GLP-1 and GIP, namely GLP-1(9−36) and GIP(3−42) previously considered largely inactive, may directly impact pancreatic morphology, with an important protective effect on beta cell health under conditions of beta cell stress.

增量激素--胰高血糖素样肽-1(GLP-1)和葡萄糖依赖性胰岛素促性多肽(GIP)会被二肽基肽酶-4(DPP-4)迅速降解为其主要的循环代谢产物 GLP-1(9-36) 和 GIP(3-42)。本研究调查了这些代谢物和等效的外显素分子 Ex(9-39) 对高脂饮食(HFD)喂养的小鼠的胰岛形态和组成α和β细胞可能产生的影响。雄性瑞士 TO 小鼠(6-8 周大)以高脂饮食或正常饮食(ND)饲养 4 个月,然后在 60 天内每天两次皮下注射 GLP-1(9-36)、GIP(3-42)、Ex(9-39) (25 nmol/kg bw) 或生理盐水载体(0.9% (w/v) NaCl)。对代谢参数进行监测,并对切除的胰腺组织进行免疫组化分析。服用多肽后,体重和评估的代谢指标没有变化。GLP-1(9-36)对胰腺组织的影响明显降低(p2)。
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引用次数: 0
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Peptides
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