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Induction of diabetes in zebrafish

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Read This Before You Try! 7 Steps To Healt Zebrafish (Danio rerio) have been used extensively to study developmental processes and mutant zebrafish strains have been used to examine vision disease present in humans. In this paper, we have induced hyperglycaemia in zebrafish by alternately immersing the fish in glucose solution or water

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Obesity is a major cause of type 2 diabetes mellitus (T2DM) in mammals. We have previously established a zebrafish model of diet-induced obesity (DIO zebrafish) by overfeeding Artemia. Here we.. Obesity is a major cause of type 2 diabetes mellitus (T2DM) in mammals. We have previously established a zebrafish model of diet-induced obesity (DIO zebrafish) by overfeeding Artemia. Here we created DIO zebrafish using a different method to induce T2DM. Zebrafish were overfed a commercially available fish food using an automated feeding system So far, type 1 diabetes mellitus (T1DM), T2DM, and maturity-onset diabetes of the young (MODY) have been induced by a variety of methods in zebrafish (Zang et al., 2018) Induction of Type 1 Diabetes Using Streptozotocin Intine et al. [ 12] reported that the established protocol using streptozotocin (STZ) as an inducer (STZ multiple injections at different time points) with a dose of 300 mg/kg caused an increment of blood glucose level in the zebrafish with low mortality (5%)

The first diet-induced obese (DIO) zebrafish model was reported in 2010 (Oka et al., 2010) where adult fish (3.5 months of age) were fed with 60 mg or 5 mg of freshly hatched Artemia per day for 8 weeks (150 calories vs. 20 calories) The induction of diabetes in zebrafish by means of 111 mM glucose is shown in Figure 5. At the beginning of the test, the fish showed blood glucose values of 88 mg/dL; on day 14 the fish treated with glucose showed blood glucose values of 310 mg/dL compared to the control group (water without glucose), which maintained glucose levels at 88 mg/dL The zebrafish were exposed to various alloxan concentration in half saline solution; 40 mg/100ml (40 mg), 120 ml (120 mg), 300 mg/100 ml (300 mg) and 400 mg/100 ml (400 mg) for 3 days. After induction, blood glucose levels were measured as shown in Figure 1. To optimize alloxan levels on the zebrafish Induction of DR by STZ has been observed in multiple models including mice, rabbits, pigs, rats, dogs, zebrafish, and monkeys [31, 63-70]. STZ is now generally preferred over alloxan, as it is more effective in recapitulating the diabetic disease state, though both drugs are still commonly used [ 41 ] Zebrafish genetic models of type 1 diabetes Beginning in 2007, Zebrafish genetic models began to be published as indicated in the references cited. The studies of Pisharath et al. 29 used molecular approaches in Zebrafish to ablate pancreatic beta cells of the fish thereby inducing a diabetic state

STZ has notable advantages over alloxan as chemical agents for induction of experimental diabetes, thus, is often preferred to the latter (alloxan). For instance, STZ has longer half-life (15 min against 1.5 min of alloxan). This makes it more stable in solution before and after injection into animals in the adult Zebrafish as opposed to just the larvae. Zebrafish chemically-induced models of type 1 and 2 diabetes In 2010 and 2012 studies were published that focused on adult Zebrafish and the use of streptozotocin (STZ) to ablate beta cells thereby inducing a DM/hyperglycaemic state.8,31 Due to the ablatio

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We have also generated transgenic zebrafish that conditionally express gain-of-function mutations in ATP-sensitive K + channels (K ATP-GOF) in β-cells. Following induction, these fish become profoundly diabetic, paralleling features of mammalian diabetes resulting from equivalent mutations The pathological feature of diabetes, hyperglycemia, is a result of an inadequate number and/or function of insulin producing β cells. Replenishing functional β cells is a strategy to cure the disease. Although β-cell regeneration occurs in animal models under certain conditions, human β cells are refractory to proliferation. A better understanding of both the positive and the negative.

Zebrafish and mouse embryos with severe or complete loss of HNF1B (also known as HNF1β, among these factors in hepatopancreas development may hint at their potential interactions in contributing to diabetes. We note that heat-shock induction at later stages (23 hpf or later) dramatically decreased the penetrance of the hepatopancreas. In 1943, alloxan became of interest in diabetes research when Dunn and McLetchie reported that it could induce diabetes in animals [ 4] as a result of the specific necrosis of the pancreatic beta cells [ 5 - 7 ]. The resulting insulinopenia causes a state of experimental diabetes mellitus called 'alloxan diabetes' [ 4, 8, 9 ] Islet inflammation is an important etiopathology of type 2 diabetes; however, the underlying mechanisms are not well defined. Using complementary experimental models, we discovered RIPK3-dependent IL1B induction in β cells as an instigator of islet inflammation. In cultured β cells, ER stress activated RIPK3, leading to NF-kB-mediated proinflammatory gene expression. In a zebrafish muscle.

In our experiments, diabetes was reliably induced by a single intravenous injection of streptozotocin dissolved in citrate buffer in the tail vein, at a dose of 65 mg/kg body weight We have cloned a second insulin gene in zebrafish and studied temporal and spatial expression of two zebrafish insulin genes. Zebrafish insulin-a (insa) and -b (insb) mRNAs are derived from two different DNA contigs on chromosomes 5 and 14, respectively, representing two different insulin genes.Real-time PCR studies suggest that insa is a maternal and also a postzygotic transcript Adult zebrafish have also been used as an obesity model. The first diet-induced obese (DIO) zebrafish model was reported in 2010 ( Oka et al., 2010) where adult fish (3.5 months of age) were fed with 60 mg or 5 mg of freshly hatched Artemia per day for 8 weeks (150 calories vs. 20 calories) Abstract. A standard protocol to develop type 1 diabetes in zebrafish is still uncertain due to unpredictable factors. In this study, an optimized protocol was developed and use

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Diabetes Induction Contact Complication; Ablation of ß-cells in Tg(ins:NTR-mCherry) transgenic zebrafish using metronidazole: Rieger, Sandra . Dechorionation of zebrafish embryos with Pronase for metronidazole-mediated ß-cell ablation: Rieger, Sandra . High Dose STZ Induction Protocol: Brosius, Fran Abstract. A standard protocol to develop type 1 diabetes in zebrafish is still uncertain due to unpredictable factors. In this study, an optimized protocol was developed and used to evaluate the anti-diabetic activity of Psychotria malayana leaf Recently, zebrafish has shown the potential to become an important in vivo model for diabetes-related research. In this study, we performed a validation study for the establishment of optimal hyperglycemia involving the following factors: alloxan concentrations of 100, 200, 300, and 400 mg/100 ml; exposure times of 30, 60, 120, and 180 min to an alloxan solution and water glucose solution; and.

Induction of hyperglycaemia in zebrafish (Danio rerio

  1. For adult induction, fish were transferred to glass beakers (7 fish/500 mL) with air stones and placed in a 37°C water bath for 3 hr/day for 2-10 days. Animal lines and maintenance Beta‐cell excitability and excitability‐driven diabetes in adult Zebrafish islets.
  2. Furthermore, RA may have a direct role in dorsal bud induction, as both mice and zebrafish deficient in RA signaling lack the dorsal pancreas [14,15]. Induction of the dorsal and ventral pancreatic buds. The pancreas is derived from the merger of distinct buds that are induced dorsally and ventrally from the foregut endoderm by the adjacent.
  3. Time-dependent metronidazole induction of β-cell-specific ROS.(a) Schematic of MTZ treatments and imaging. Zebrafish (NTR +) larvae were treated with MTZ or vehicle for 0, 1, 3, 6, 12, or 24 hours with a staggered start such that all treatments were completed simultaneously; larvae were then incubated with CellROX green stain at 105 hpf and fixed/analyzed at 106 hpf
  4. Here, we report that glucose metabolism impacts the onset and magnitude of HSC induction in vivo. In zebrafish, transient elevations in physiological glucose levels elicited dose-dependent effects on HSC development, including enhanced runx1 expression and hematopoietic cluster formation in the aorta-gonad-mesonephros region; embryonic-to-adult.
  5. Zebrafish 2010; 7: 205-213 ; 4 Olsen AS, Sarras Jr MP, Intine RV. Limb regeneration is impaired in an adult zebrafish model of diabetes mellitus. Wound Repair Regen 2010; 18: 532-542 ; 5 Gleeson M, Connaughton V, Arneson LS. Induction of hyperglycaemia in zebrafish (Danio rerio) leads to morphological changes in the retina. Acta Diabetol 2007.
  6. DR can be studied in zebrafish via direct elevation of glucose in the surrounding as well as angiogenesis without the involvement of glucose. 2.8.1. Glucose-Induced Diabetic Model of DR. In brief, zebrafish was exposed to freshwater with alternation between 2% and 0% glucose in every 24 hours for 30 days [ 238
  7. Regeneration-competent species possess the ability to reverse the progression of severe diseases by restoring the function of the damaged tissue. However, the cellular dynamics underlying this capability remain unexplored. Here, we use single-cell transcriptomics to map the cellular dynamics underlying de novo β-cell regeneration during induction and recovery from diabetes in zebrafish

Gleeson, M., Connaughton, V., Arneson, L. S. Induction of hyperglycaemia in zebrafish (Danio rerio) leads to morphological changes in the retina. Acta Diabetol. 44, (3), 157-163 (2007). Jorgens, K., et al. High tissue glucose alters intersomitic blood vessels in zebrafish via methylglyoxal targeting the VEGF receptor signaling cascade. Diabetes After the publication of Oka et al., several other methods of inducing obesity in zebrafish were applied as an induction by overfeeding with Artemia saline or commercial feed or through a hypercaloric diet with corn oil or commercial oil-enriched feed for different purposes of the study on obesity [7, 28, 29, 30] Induction Streptozotocin with High Fat Diet Timelines Induction: Day (-14) to Day 0; Dosing: Day 7-14; Readout: Day 10, 14 Study Arms (n = 24) Wild Type, Model, Standard (Metformin), Dilution 1, 2 and 3 Read Outs Phenotype •Weight Loss •Fatigue •Abnormal Blood Sugar Serum Biochemistry •Neutrophils •GAD65 AutoAntibodies •T Cell Volume Cytology •Cytology of Nephrons, Neurons and.

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Induction of hyperglycaemia in zebrafish ( Danio rerio

Short-term overfeeding of zebrafish with normal or high-fat diet as a model for the development of metabolically healthy In summary, we have established a method for the specific induction of metabolically distinct obesity hepatic steatosis and type 2 diabetes [4-6]. Compared to the metabolically healthy obese (MHO) phenotype, which. In this article, we report differences in hyperglycemia induction and maintenance in young (4-11 months) versus old (1-3 years) zebrafish adults. In particular, older fish immersed in an alternating constant external glucose solution (2%) for 2 months displayed elevated blood glucose levels for the entire experimental duration Type 1 diabetes is caused by the body incorrectly destroying the cells in the pancreas—known as β cells—that produce insulin and so control the amount of sugar found in the bloodstream. Drugs that increase the rate at which new β cells form could therefore help to treat this disease. High-throughput screening is a technique that uses automated systems to rapidly test the effects of large.

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Development of a Novel Zebrafish Model for Type 2 Diabetes

The zebrafish has evolved as a model for diabetes research in the past decade (27, 28). Glucose homeostasis in zebrafish is very similar to humans and other mammals and glucose-induced alterations of the retina (29), kidney (30), and neuronal tissue (31) have been shown to develop in adult zebrafish Specifically, the conserved aspects of zebrafish innate immune responses relative to mammalian systems, together with the ease of genetic manipulation of the model system, make the zebrafish a powerful in vivo model for studying the effects of excessive cytokine induction (van der Vaart et al., 2012). To date, no models of tissue-specific. This study aimed to identify the effectiveness of SNEDDS of Pegagan Leaf Ethanol Extract (PLE) to reduce fasting blood glucose (FBG) levels in zebrafish. Centella asiatica (L.) Urb. or pegagan is among the medicinal plants widely used to treat diabetes in Indonesia. Maceration was employed with 70% ethanol to obtain a viscous extract for the formulation of SNEDDS with Capryol 90, Tween 80, and.

Fluorescent microscope images of DNA of Zebrafish treated

Because chronic hyperglycaemia is a feature of human type 2 diabetes, we hypothesized that adequate exposure to HG conditions would induce metabolic disturbances that are similar to DR models. Thus, retinal vascular changes in HG zebrafish may reflect similar changes observed in mammalian models Induction of self-replication of existing β-cells is a potential treatment for diabetes. In zebrafish larvae, β-cells rarely self-replicate, even under conditions that favor β-cell genesis such overnutrition and β-cell ablation. It is not clear why larval β-cells are refractory to replication In summary, we have established a method for the specific induction of metabolically distinct obesity phenotypes in zebrafish. Our results indicate that zebrafish represents an attractive model to study regulatory mechanisms involved in the determination of AT phenotype during development of metabolically healthy versus metabolically unhealthy. Abstract. Type 2 diabetes mellitus is characterized by insulin resistance. However, the complete molecular mechanism remains unclear. In this study, zebrafish were fed a long-term high-fat diet to induce type 2 diabetes, which resulted in a higher body weight, body mass index, more lipid vacuoles in liver, increased insulin transcription level in liver, brain and muscle, and high fasting blood.

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Existing methods for induction of diabetes in rodents using STZ. the recent emergence of zebrafish can resolve this complication. Zebrafish is extensively used in the study of visual development and impairments owing to its similarity to those seen in human [236] PLEXIN D1 ( PLXND1 ) has been implicated in body fat distribution and type 2 diabetes by genome-wide association studies, but the mechanism is unknown. We show here that Plxnd1 regulates body fat distribution in zebrafish by controlling the visceral adipose tissue (VAT) growth mechanism. Plxnd1 deficiency in zebrafish resulted in induction of a hyperplastic state and reduced lipid deposition. Induction of TNBS- enterocolitis in adult zebrafish. Wild-type 3-6 month old male zebrafish were purchased from EkkWill Waterlife (Ruskin, FL, USA) and kept in the zebrafish facility for at least one month for equilibration prior to induction of colitis studies in zebrafish. Induction of TNBS- enterocolitis in adult zebrafish Wild-type 3-6 month old male zebrafish were purchased from EkkWill Waterlife (Ruskin, FL, USA) and kept in the zebrafish facility for at least one month for equilibration prior to induction of colitis. Myeloperoxidase-GFP transgenic (Tg(mpx:EGFP)

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Frontiers Which Hyperglycemic Model of Zebrafish (Danio

Wnt signaling or Hnf1b function. Using a novel hypomorphic hnf1ba zebrafish mutant that exhibits pancreas hypoplasia, as observed in HNF1B monogenic diabetes, we show that hnf1baplays essential roles in regulating -cell number and pancreas specification,β distinct from its function in regulating pancreas size and liver specification, respectively The zebrafish (Danio rerio) is a freshwater fish belonging to the minnow family of the order Cypriniformes.Native to South Asia, it is a popular aquarium fish, frequently sold under the trade name zebra danio (and thus often called a tropical fish although both tropical and subtropical).. The zebrafish is an important and widely used vertebrate model organism in scientific research, for. DG and Metformin commences after 28 days of induction of diabetes. 1mg DG was weighed and allowed to dissolve in BG oil. Dose of each Protective role of diosgenin against hyperglycaemia-mediated cerebral ischemic brain injury in zebrafish model of type II diabetes mellitus. Zebrafish CYP3A65 (Tseng et al. 2005) and human CYP3A4, CYP3A5, and CYP3A7 (Maruyama et al. 2007) show similar induction patterns in the liver. In humans, CYP3A4 efficiently metabolizes E 2 similar to the CYP1As (Lee et al. 2003), while zebrafish CYP3A65 poorly metabolizes E 2 at rates that are similar to human CYP3A5 and CYP3A7 (Lee et al. 2003) Diabetes‐induced retinal vessel leakage and the protective effect of resveratrol treatment. Fluorescence angiography demonstrated vessel leakage in the peripheral and the central regions in mouse retinas 2 months after induction of diabetes (arrows and arrowheads, Fig. 1B,D) compared with controls, but administration of resveratrol prevented these changes ()

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Diabetes is a morbid metabolic disorder that affects almost 500 million people worldwide. Although multiple factors contribute to diabetes pathogenesis, pancreatic islet inflammation and dysfunction are shared characteristics of its major forms. 12- lipoxygenase (12-LOX), an enzyme involved in lipid metabolism, has been implicated in islet inflammation. 12-LOX generates reactive oxygen species. Author Summary Fatty liver disease (steatosis) is the most common liver disease worldwide and is commonly caused by obesity, type 2 diabetes, or alcohol abuse. All of these conditions are associated with impaired hepatocyte protein secretion, resulting in hypoproteinemia that contributes to the systemic complications of these diseases. The unfolded protein response (UPR) is activated in. Stanford Diabetes Work-In-Progress Seminar Series . Participants: Tolerance induction in islet transplantation CRISPR generated KATP channel mutation as a neonatal diabetes model in zebrafish SUMMER BREAK: Series will return in September via Zoom only Zebrafish embryos were used in this study because the innate immune system of the zebrafish is active from birth and is the only means of defense during the first 3 days of development. This system is functionally as efficient in embryos as it is in adults, and the adaptive immune system is not completely functional until the fourth to sixth. The zebrafish has evolved as a model for diabetes research in the past decade (27, 28). Glucose homeostasis in zebrafish is very similar to humans and other mammals and glucose-induced alterations of the retina ( 29 ), kidney ( 30 ), and neuronal tissue ( 31 ) have been shown to develop in adult zebrafish

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Frontiers Zebrafish as a Model for Obesity and Diabetes

The ER stress and autophagy-induction findings in zebrafish were validated in 2 mouse models of porphyria: the FECH knockout model and a subacute porphyria model that involves 5 d of DDC feeding. In both models, porphyrin accumulation (Fig. 6 C ) was associated with increased nuclear CHOP and ATF4, as well as increased LC3B-II levels (relative. Nephropathy. Animal models have been developed to examine the immunological aspects of type 1 diabetes and the pathogenic mechanisms associated with diabetic retinopathy, but the methods of diabetes induction raise zebrafish to either a 2% or 0% glucose solution, alternat- Read Document Obesity induction in adult zebrafish leads to negative reproduction and offspring effects in Reproduction Authors: Bárbara do Carmo Rodrigues Virote 1 , Amanda Maria Siqueira Moreira 1 , José Gilmar da Silva Souza 2 , Tássia Flávia Dias Castro 2 , Naiara Melo 2 , William Franco Carneiro 2 , Cristina Delarete Drummond 3 , André Rodrigues da. 2.3.1. Step 1: Cardiac Hypertrophy Induction in D. rerio Inducer stock of erythromycin was prepared by dissolving it at the concentration of 2 mg/mL in 0.9% saline solution and was stored at 20 C until further use. For the induction of CH, 50 L of the stock solution (100 g of erythromycin) was added to 4 L of the housing water of D. rerio

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Queen Mary, University of London. (2011, July 4). Zinc and the zebrafish: Fluorescent fish could hold key to understanding diabetes and other diseases. ScienceDaily. Retrieved June 18, 2021 from. In contrast, zPDX#B2 showed a significant induction of activated Caspase3 (1.6-fold induction, P = .0007), indicating that apoptosis was triggered by CRT (Fig. 6j-m). Albeit with only two patients our results constitute a proof-of-principle that the zebrafish Avatar assay was able to predict the clinical response to CRT

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Although the mouse remains the main animal model for studying metabolic diseases, such as diabetes, zebrafish (Danio rerio) have also become more popular for investigating the development of the pancreas 9-12, as well as the pathologies associated with diabetes 13-16. Zebrafish adults breed year‐round, and the embryos develop ex utero and are. Studies in zebrafish and rodents have shown a significant dose-dependent increase in blood glucose levels after acrylamide exposure (6-8). High fasting plasma glucose (FPG) is an important indicator for diabetes and the third leading risk factor for global disease burden, accounting for 6.53 million deaths . However, epidemiological study of. Heat induction of the constitutively active zebrafish Notch1 receptor intracellular domain (NICD) via a Gal4/UAS transgenic system 26 expands HSCs in the AGM as shown by expansion of c-myb and runx1 transcripts (Figure 4A,B). 8 To knock down tbx16 or plcγ1 translation, gene-specific morpholinos (MO) 33 were injected into embryo clutches. Introduction. The zebrafish model system is becoming one of the most widely used animal models for developmental research because of its fecundity and its genetic and physiological similarities to mammals (Vascotto et al. 1997, Parng et al. 2002).These advantages are leading to the use of the zebrafish model in drug discovery and toxicological screening

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Zebrafish offer a new and versatile model to study through characterising the induction of IL-1β in response to injury myocardial infarction), type 2 diabetes and osteoarthritis. Based on in vitro experiments, IL-1 is thought to be released into the circulation an Zebrafish DCM models have also been generated through pharmacological induction by administering the K + channel blocker terfenadine to embryos (Gu et al., 2017), whereas a zebrafish model of ACM was developed using cardiomyocyte-driven expression of a plakoglobin disease variant, resulting in cardiomegaly and thinning of atrial and ventricular. This approach requires a thorough understanding of the temporal sequence of the signaling events underlying pancreatic β-cell induction during embryonic development. The zebrafish system has emerged as a powerful tool in the study of pancreas development

Diabetes mellitus-induced hyperglycemia is associated with a number of pathologies such as retinopathy, nephropathy, delayed wound healing and diabetic peripheral neuropathy (DPN). Approximately 50% of patients with diabetes mellitus will develop DPN, which is characterized by disrupted sensory and/or motor functioning, with treatment limited to pain management. Zebrafish (Danio Rerio) are an. Zebrafish mutations and functional analysis of the vertebrate genome. As the first draft of the human genome nears completion, we are faced with the challenge of defining the functions of the 70,000-100,000 genes contained within the sequence. A powerful combination of large-scale forward genetics and elegant cellular analysis ensures that. The number of people with diabetes is approaching 500 million. It is a disease that can be debilitating to patients and their families. such as type 1 diabetes. Following induction of pluripotency, stem cell differentiation protocols can program iPS cells into the desired target cell. Zebrafish embryos are also highly amenable to. Thus, while induction of ER stress and oxidative stress both lead to hepatic steatosis, the changes in gene expression are distinct, with the increase in lipogenic genes from oxidative stress similar to the changes induced by fructose. Torc1 Axis Is Up-Regulated in Zebrafish Models of Hepatic Steatosi