Relevant bibliographies by topics / Non-insulin-dependent diabetes – Animal models

Academic literature on the topic 'Non-insulin-dependent diabetes – Animal models'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Non-insulin-dependent diabetes – Animal models.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Non-insulin-dependent diabetes – Animal models"

1

Shafrir, Eleazar. "Animal models of non-insulin-dependent diabetes." Diabetes / Metabolism Reviews 8, no. 3 (October 1992): 179–208. http://dx.doi.org/10.1002/dmr.5610080302.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Pierce, G. J., T. G. Maddaford, and J. C. Russell. "Cardiovascular dysfunction in insulin-dependent and non-insulin-dependent animal models of diabetes mellitus." Canadian Journal of Physiology and Pharmacology 75, no. 4 (April 1, 1997): 343–50. http://dx.doi.org/10.1139/y97-027.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Wong, F. Susan, and Charles A. Janeway. "Insulin-dependent diabetes mellitus and its animal models." Current Opinion in Immunology 11, no. 6 (December 1999): 643–47. http://dx.doi.org/10.1016/s0952-7915(99)00031-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Peterson, Jeffrey D., and Kathryn Haskins. "Immunotherapy of animal models of insulin-dependent diabetes mellitus." Current Opinion in Endocrinology and Diabetes 2, no. 1 (February 1995): 17–23. http://dx.doi.org/10.1097/00060793-199502000-00004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Miyazaki, J. I., and F. Tashiro. "Transgenic Models of Insulin-Dependent Diabetes Mellitus." ILAR Journal 35, no. 2 (January 1, 1993): 37–41. http://dx.doi.org/10.1093/ilar.35.2.37.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Bohlen, H. G., and J. M. Lash. "Endothelial-dependent vasodilation is preserved in non-insulin-dependent Zucker fatty diabetic rats." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 6 (June 1, 1995): H2366—H2374. http://dx.doi.org/10.1152/ajpheart.1995.268.6.h2366.

Full text
Abstract:
Alterations in the structural properties of the microvasculature and in vasodilation mediated by endothelial- and, to some extent, nonendothelial-dependent mechanisms occurs in insulin-dependent diabetic humans and animals. Less severe problems of this type appear to occur during non-insulin-dependent diabetes mellitus (NIDDM) in humans, but data based on animal models of NIDDM are not available. The endothelial- and nonendothelial-mediated dilation of intestinal arterioles was studied in insulin-resistant male Zucker fatty diabetic (DB) rats and their lean normal male littermates (LM) at ages 22-25 and 35-40 wk. DB become hyperglycemic (450-550 mg/100 ml) at age 9-10 wk. Microiontophoretic release of acetylcholine, ADP, and nitroprusside onto arterioles caused equivalent dilation in LM and DB for both large and intermediate diameter arterioles. Administration of streptozotocin (STZ) to DB at age 18-19 wk lowered their insulin concentration approximately 25% but did not significantly effect the resting plasma glucose concentration. However, endothelial-dependent vasodilation was attenuated by 70-80% within 8-10 wk. The overall results indicate that prolonged hyperglycemia in insulin-resistant but hyperinsulinemic rats does not impair the endothelial- and nonendothelial-dependent dilation of the intestinal microvasculature. However, compromising beta-cell function with STZ, as indicated by lowering the insulin concentration by one-fourth, substantially compromises endothelial-dependent dilation similar to that found in insulin-dependent diabetic rats and humans.
APA, Harvard, Vancouver, ISO, and other styles
7

Fabregat, M. E., A. Novials, M. H. Giroix, A. Sener, R. Gomis, and W. J. Malaisse. "Pancreatic Islet Mitochondrial Glycerophosphate Dehydrogenase Deficiency in Two Animal Models of Non-Insulin-Dependent Diabetes Mellitus." Biochemical and Biophysical Research Communications 220, no. 3 (March 1996): 1020–23. http://dx.doi.org/10.1006/bbrc.1996.0525.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Takeshita, Noritaka, Hitoshi Ishida, Taizo Yamamoto, Gyohan Koh, Takeshi Kurose, Kazuo Tsuji, Yoshimasa Okamoto, Hitoshi Ikeda, and Yutaka Seino. "Circulating levels and bone contents of bone γ-carboxyglutamic acid-containing protein in rat models of non-insulin-dependent diabetes mellitus." Acta Endocrinologica 128, no. 1 (January 1993): 69–73. http://dx.doi.org/10.1530/acta.0.1280069.

Full text
Abstract:
In order to investigate the pathophysiology of the diabetic osteopenia observed in non-insulin-dependent diabetes mellitus, the circulating levels and the bone contents of bone γ-carboxyglutamic acid-containing protein (osteocalcin) were determined in rat models of non-insulin-dependent diabetes mellitus, neonatally streptozotocin-induced rats and in genetic Wistar fatty rats. In Wistar fatty rats the plasma level of osteocalcin was 8.1±0.8 nmol/l, significantly lower than the value of 1 7.3±0.9 nmol/l in their lean littermates (p<0.001). Bone length, bone strength, and weight of powdered bone in Wistar fatty rats were significantly decreased compared to control rats (p<0.001, p<0.02 and p<0.001, respectively). Bone content of osteocalcin per femur in Wistar fatty rats was also significantly decreased compared to controls (p<0.001). In addition, plasma osteocalcin in neonatally streptozotocin-induced diabetic rats was 2.9±0.3 nmol/l, which was also significantly decreased compared to the value of 5.6±0.5 nmol/l in their controls (p<0.001). Since it has been established that the plasma level of osteocalcin is well related to bone formation and turnover, the low plasma values in these animal models suggest that bone formation and turnover are decreased in non-insulin-dependent diabetes mellitus. Low bone formation and turnover are, therefore, postulated to be one of the pathophysiological characteristics of the skeletal tissue in non-insulin-dependent diabetes mellitus, and to be at least in part responsible for the occurrence of this complication.
APA, Harvard, Vancouver, ISO, and other styles
9

Aleixandre de Artiñano, Amaya, and Marta Miguel Castro. "Experimental rat models to study the metabolic syndrome." British Journal of Nutrition 102, no. 9 (July 27, 2009): 1246–53. http://dx.doi.org/10.1017/s0007114509990729.

Full text
Abstract:
Being the metabolic syndrome a multifactorial condition, it is difficult to find adequate experimental models to study this pathology. The obese Zucker rats, which are homozygous for the fa allele, present abnormalities similar to those seen in human metabolic syndrome and are a widely extended model of insulin resistance. The usefulness of these rats as a model of non-insulin-dependent diabetes mellitus is nevertheless questionable, and they neither can be considered a clear experimental model of hypertension. Some experimental models different from the obese Zucker rats have also been used to study the metabolic syndrome. Some derive from the spontaneously hypertensive rats (SHR). In this context, the most important are the obese SHR, usually named Koletsky rats. Hyperinsulinism, associated with either normal or slightly elevated levels of blood glucose, is present in these animals, but SHR/N-corpulent rats are a more appropriated model of non-insulin-dependent diabetes mellitus. The SHR/NDmc corpulent rats, a subline of SHR/N-corpulent rats, also exhibit metabolic and histopathologic characteristics associated with human metabolic disorders. A new animal model of the metabolic syndrome, stroke-prone–SHR (SHRSP) fatty rats, was obtained by introducing a segment of the mutant leptin receptor gene from the Zucker line heterozygous for the fa gene mutation into the genetic background of the SHRSP. Very recently, it has been developed as a non-obese rat model with hypertension, fatty liver and characteristics of the metabolic syndrome by transgenic overexpression of a sterol-regulatory element-binding protein in the SHR rats. The Wistar Ottawa Karlsburg W rats are also a new strain that develops a nearly complete metabolic syndrome. Moreover, a new experimental model of low-capacity runner rats has also been developed with elevated blood pressure levels together with the other hallmarks of the metabolic syndrome.
APA, Harvard, Vancouver, ISO, and other styles
10

Freund, P., H. P. Wolff, and H. F. Kühnle. "(−)-BM 13.0913: A new oral antidiabetic agent that improves insulin sensitivity in animal models of type II (non—insulin-dependent) diabetes mellitus." Metabolism 44, no. 5 (May 1995): 570–76. http://dx.doi.org/10.1016/0026-0495(95)90112-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Non-insulin-dependent diabetes – Animal models"

1

Lau, Tik-yan Ivy, and 劉荻茵. "Macrophage-adipocyte cross-talk in the initiation of obesity-related insulin resistance and type 2 diabetes: roleof adiponectin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B4129046X.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Clark, Catherine Renee. "Thyroid hormone influence on oxygen consumption rates, body mass, and lipid metabolism in mice with noninsulin dependent diabetes mellitus." CSUSB ScholarWorks, 1995. https://scholarworks.lib.csusb.edu/etd-project/1025.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Black, Shawn Clive. "Studies on the effect of experimental insulin-dependent diabetes mellitus and hypothyroidism on rat cardiac and saroplasmic reticulum function." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30597.

Full text
Abstract:
The objective of these studies was to investigate mechanisms whereby cardiac sarcoplasmic reticulum (SR) calcium transport activity may be influenced by changes in the lipid environment of the SR membrane in the experimental endocrine disease states hypothyroidism and insulin-dependent diabetes mellitus. These endocrine disease states were studied to determine, respectively, if SR function is influenced by endogenous acylcarnitine associated with the SR membrane and if SR phospholipid acyl composition plays a role in diabetes-induced cardiomyopathy. The effects of endogenous acylcarnitines on SR calcium transport in hypothyroidism were of interest since it has previously been implicated that acyl carnitines play a regulatory role in SR function. SR calcium transport was not affected at two weeks, but was significantly reduced at four, six and eight weeks following thyroidectomy. Endogenous acyl carnitines were detectable in the SR membrane fraction isolated from both euthyroid control and thyroidectomized animals. The level of acyl carnitine associated with the SR did not correlate with calcium transport activity. Since acylcarnitine did not appear to play a role in the reduced SR calcium transport, SR calcium pump protein was quantified. The reduced SR calcium transport of thyroidectomized animals, manifest at four weeks, was shown to correlate with a reduction in SR acylphosphoprotein level. Therefore the reduced SR calcium transport activity of hypothyroidism is not related to the level of SR acyl carnitine, but rather a hypothyroid-induced reduction in SR calcium pump sites. Since omega-3 fatty acids affect parameters relevant to diabetes-induced cardiomyopathy, it was of interest to determine the cardiac effects of omega-3 fatty acid treatment of streptozocin (STZ)-induced diabetic animals. Omega-3 fatty acid treatment significantly reduced the development of diabetic cardiomyopathy and improved isolated cardiac SR calcium transport activity of STZ-induced diabetic animals. To determine if the cardiac and SR changes were related to membrane changes induced by omega-3 fatty acids, the fatty acyl composition of phospholipid was determined. Phospholipid analysis of cardiac phosphatidylcholine and phosphatidylethanolamine, and total SR phospholipid indicated modest changes in the omega-3 fatty acid component. Omega-3 fatty acid treatment produced slight (statistically insignificant) changes in SR cholesterol levels. Therefore a change in membrane phospholipid acyl composition may not account for the observed cardiac and SR functional changes.
Pharmaceutical Sciences, Faculty of
Graduate
APA, Harvard, Vancouver, ISO, and other styles
4

Jiao, Hong. "Genetic dissection of multifactorial disease models in the rat /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-287-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Kergoat, Micheline. "Secretion et mode d'action de l'insuline dans un modele de diabete non-insulinodependant chez le rat." Paris 7, 1988. http://www.theses.fr/1988PA077085.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Morrice, Nicola. "Endocrine and genomic analysis of Fenretinide-mediated retinoic acid receptor signalling in models of obesity and type-2 diabetes." Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=232274.

Full text
Abstract:
Obesity and type-2 diabetes are major global health crises. The synthetic retinoid compound 4-hydroxy(phenyl)retinamide (Fenretinide, FEN), has been shown to inhibit adiposity and reverse insulin resistance in pre-clinical studies. Fenretinide acts via several different mechanisms, including induction of retinoid signalling and increased hepatic lipid oxidation to exert its metabolic effects. However, the signalling mechanisms behind these effects have yet to be fully elucidated. A number of approaches were taken in this thesis to investigate the signalling mechanisms of Fenretinide. To characterise the relationship between Fenretinide and leptin signalling, Fenretinide treatment was administered in two different leptin-deficient mouse models. Fenretinide effects on hepatic signalling mechanisms were further characterised by performing global transcriptomics analysis in liver from mice receiving HFD ± Fenretinide. In this analysis, the important metabolic hormone fibroblast growth factor (FGF) 21 was identified as a novel retinoid-dependent target of Fenretinide signalling, which was further characterised in multiple mouse models. Retinoic-acid receptor-specific ChIP-sequencing was performed in order to identify other liver genes that are regulated by Fenretinide via retinoid-dependent signalling mechanisms. This work has shown that the beneficial effects of Fenretinide on adiposity occur via a mechanism independent of that through which Fenretinide mediates effects on glucose homeostasis. Fenretinide effects on insulin sensitivity and glucose homeostasis are most likely mediated via the inhibition of ceramide synthesis in the liver and other metabolically active tissues. This work also shows that Fenretinide can normalise the effects of chronic HFD-feeding by targeting the expression of a set of PPARα-target genes in the liver via a retinoid-dependent signalling mechanism. Overall, the work described in this thesis both uncovers more detail about the signalling mechanisms of Fenretinide and identifies novel target genes that may be exploited for the development of new therapeutics to treat obesity and type 2 diabetes.
APA, Harvard, Vancouver, ISO, and other styles
7

Kharroubi, Ilham. "Molecular pathways underlying beta-cell loss in vitro models of type 2 diabetes mellitus." Doctoral thesis, Universite Libre de Bruxelles, 2006. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210746.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Dable, Velho Gilberto. "Developpement d'un capteur de glucose implantable et application a des etudes de diabetologie experimentale." Paris 7, 1988. http://www.theses.fr/1988PA077044.

Full text
Abstract:
Application du capteur de glucose sous forme d'aiguille a une methode originale de fixation de l'enzyme glucose oxydase, a l'etude de la cinetique in vitro du transfert de glucose dans un modele de pancreas bioartificiel et a l'etude cinetique de la concentration peritoneale de glucose chez le rat
APA, Harvard, Vancouver, ISO, and other styles
9

Quiniou, Debrie Marie-Christine. "Immunité anti-ilots chez des diabétiques insulino-dépendants de type 1." Paris 6, 1986. http://www.theses.fr/1986PA066085.

Full text
Abstract:
La destruction sélective des cellules bêta des ilots de Langerhans pourrait être due à une réaction immunitaire dirigée contre elles. Etude de la phase effectrice de la réponse auto-immune c'est-à-dire l'immunité cellulaire, l'immunité humorale complément dépendante, la cytotoxicité cellulaire dépendante d'anticorps chez les diabétiques de type 1. L'évolution de ces paramètres a été étudiée en fonction de la durée clinique de la maladie et de la présence ou de l'absence de manifestations auto-immunes extra-pancréatiques.
APA, Harvard, Vancouver, ISO, and other styles
10

Boey, Dana School of Medicine UNSW. "The role of PYY in regulating energy balance and glucose homeostasis." 2007. http://handle.unsw.edu.au/1959.4/40835.

Full text
Abstract:
Peptide YY (PYY) is a gut-derived hormone that is renowned for its effects on satiety. Reduced satiety in obese people has been attributed to low fasting and postprandial PYY levels. However, it has not been determined whether low PYY levels are the cause or the outcome of obesity. Moreover, the long-term role of PYY in regulating energy balance is unclear. Results presented in this thesis, using PYY-deficient mice (PYY-/-) and PYY transgenic mice (PYYtg) highlight that PYY indeed has an important role in regulating energy balance and glucose homeostasis in vivo. PYY knockout mice became obese with ageing or high-fat feeding linked to a hyperinsulinemic phenotype associated with hypersecretion of insulin from isolated pancreatic islets. These findings suggested that PYY deficiency may be a predisposing factor for the development of obesity and type 2 diabetes. On the other hand, PYYtg mice exhibited decreased adiposity and increased metabolism under high-fat feeding. Furthermore, PYYtg/ob mice had improved glucose tolerance and decreased adiposity. These latter studies suggested that high circulating PYY levels may protect against the development of obesity and type 2 diabetes. Interestingly, both animal models support PYY as an important regulator of the somatotropic axis. These preliminary findings prompted investigations in understanding whether low PYY levels may be a predisposing factor for the development of obesity and type 2 diabetes in human subjects. In a population of healthy human subjects that had a predisposition to the development of type 2 diabetes and obesity, fasting PYY levels were lower than in normal subjects. Moreover, low fasting PYY levels strongly correlated with decreased insulin sensitivity and high levels of fasting insulin. Collectively, these findings suggest that low circulating levels of PYY could contribute to increased adiposity, insulin resistance and type 2 diabetes. Therefore determination of PYY levels may be a method of detecting whether people are predisposed to becoming obese and insulin resistant. This work also suggests that treatments that enhance circulating PYY levels may be protective in the development of obesity and type 2 diabetes.
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Non-insulin-dependent diabetes – Animal models"

1

1927-, Schäfer Harald, and Titlbach Milan 1928-, eds. Histophysiology of the obesity-diabetes syndrome in sand rats. Berlin: Springer-Verlag, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Edward, Leiter, and Atkinson Mark 1961-, eds. NOD mice and related strains: Research applications in diabetes, AIDS, cancer, and other diseases. Austin, Tex: R.G. Landes, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Seiichirō, Tarui, Tochino Yoshihiro, and Nonaka Kyohei, eds. Insulitis and type I diabetes: Lessons from the NOD mouse. Tokyo: Academic Press, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ulrike, Beisiegel, Joost Hans-Georg, and SpringerLink (Online service), eds. Sensory and Metabolic Control of Energy Balance. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

1914-, Cohen A. M., and Rosenmann E. 1931-, eds. The Cohen diabetic rat. Basel: Karger, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Current concepts of a new animal model: The NON mouse. Amsterdam: Elsevier, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Sakamoto, N., and N. Hotta. Current Concepts of a New Animal Model: The Non Mouse. Elsevier Publishing Company, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Titlbach, Milan, Harald Schäfer, and Herwig Hahn von Dorsche. Histophysiology of the Obesity-Diabetes Syndrome in Sand Rats. Springer London, Limited, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

F, Howard Charles, and American Society of Primatologists. Meeting, eds. Nonhuman primate studies on diabetes, carbohydrate intolerance, and obesity. New York: A.R. Liss, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

(Editor), Edward Leiter, and Mark Atkinson (Editor), eds. Nod Mice and Related Strains: Research Applications in Diabetes, AIDS, Cancer, And Other Diseases (Molecular Biology Intelligence Unit). Landes Bioscience, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Non-insulin-dependent diabetes – Animal models"

1

Bieg, Sabine, and Åke Lernmark. "Animal Models for Insulin-Dependent Diabetes Mellitus." In Autoimmune Endocrinopathies, 113–39. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-704-8_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Leahy, J. L., S. Bonner-Weir, and G. C. Weir. "Rat Models of Non-Insulin-Dependent Diabetes Mellitus: Evidence that Mild Increases in Plasma Glucose Play an Important Role in Pathogenesis." In The Pathology of the Endocrine Pancreas in Diabetes, 285–309. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-72691-0_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ehlers, M., C. Papewalis, S. Schinner, HS Willenberg, WA Scherbaum, and M. Schott. "New Link between the Innate and the Adaptive Immune System in Two Animal Models of Insulin-Dependent Diabetes." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–467—P1–467. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p10.p1-467.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Veronique, Traynard, Yuen Muk Wing, and Drapeau Christian. "Seabuckthorn Polyphenols: Characterization, Bioactivities and Associated Health Benefits." In Phenolic Compounds [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98706.

Full text
Abstract:
Sea Buckthorn (Hippophae rhamnoides) has a long history of use as food and medicine in Tibet and Northern Asia, where the plant has been associated with a wide range of health benefits. Sea buckthorn (SB) berry, seed and leaf have been reported to contain more than 190 bioactive compounds, including polyphenols (epicatechin, epigallocatechin, gallic acid, proanthocyanidins, chloregenic acid) and flavonoids (quercetin, isorhamnetin, kampferol glycosides, lutoelin, myricetin). SB represents a good source of phenolic compounds and flavonoids acting in synergy with PUFA such as omegas 3, 6, 7 and 9, vitamins (vitamin C), and organic acids. SB exerts antioxidant, anti-inflammatory, cytoprotective, anti-cancer, hepatoprotective properties, associated with improvement in various metabolic markers such as glycemic control and lipid profile. SB polyphenol fraction also demonstrated significant cardioprotective, antihypertensive and neuroprotective actions. SB acts as a natural stem cell mobilizer associated with significant regenerative properties. As a consequence, SB polyphenol consumption stimulates pancreatic regeneration in animal model of insulin-dependent diabetes. In conclusion, SB polyphenols exert a wide range of health benefits in metabolic health including obesity, diabetes and hypertension, as well as liver, kidney and brain health, positioning sea buckthorn berry extract as an interesting and valuable dietary supplement for natural complementary therapy and for antiaging.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Non-insulin-dependent diabetes – Animal models' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography