The Nile Rat (Arvicanthis niloticus) as a Superior Carbohydrate-Sensitive Model for Type 2 Diabetes Mellitus (T2DM).

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Insulin 1 endocrinologydiseasesdrugs
glucose intolerance 5 endocrinologydiseases
hyperinsulinemia 12 endocrinologydiseases
cholic acid 1 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
diabetic retinopathy 6 endocrinologydiseases
hyperglycemia 27 endocrinologydiseases
hyperlipidemia 6 endocrinologydiseases
hypertriglyceridemia 1 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
obesity 17 endocrinologydiseases
testosterone 1 endocrinologydiseasesdrugs

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Insulin 70478 bySigns of Metabolic SyndromeHyperphagia with CauseIncr BP *Abdominal ObesityIncr TG *Decr HDL *Hyper Insulin emiaHuman [[2],[3],[4],[5],[20],[21],[29]]Natural (diet x gene interaction) CarbohydrateNoDiabetics,
cholic acid 52645 disruption of bile acid metabolism and tumor induction by recycled secondary bile acids, specifically deoxy cholic acid [[105],[106],[107],[108]].In addition, peripancreatic steatitis associated with ‘leaky pancreas syndrome’
testosterone 54850 the specific effects of sex hormones because symptoms in males are exacerbated during puberty (rising testosterone ), but abate somewhat in females when estrus evolves around 7–8 weeks of age. This suggests that estrogen
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diabetes mellitus 428 aluu@brandeis.edu (A.L.)Publication date (epub): 2/2018Publication date (collection): 2/2018AbstractType II diabetes mellitus (T2DM) is a multifactorial disease involving complex genetic and environmental interactions. No single
diabetic retinopathy 14651 with the chronic hyperglycemia found in humans with diabetes, rendering this model useful for studying diabetic retinopathy [[73],[74],[75],[76]].Diabetes in the SDT rat has a polygenic basis, regulated by at least seven quantitative
diabetic retinopathy 27091 adhere to the human paradigm in its etiology and pathophysiology. While the SDT is useful for studying diabetic retinopathy , it is not a true nutritional model of this condition, nor is it faithful to the etiology of human T2DM.
diabetic retinopathy 33284 [[30],[52],[99]].Furthermore, unlike humans [[36]] or Nile rats [[100],[101]], the Sand rat [[39]] reportedly does not develop diabetic retinopathy during prolonged T2DM.3. The Nile Rat (Arvicanthis niloticus)The following overview emphasizes the utility
diabetic retinopathy 35568 represent a useful nutritional model for study of diabetic lesions of the eye, including cataracts and diabetic retinopathy , and as indicated below, advanced diabetes is accompanied by renal failure [[34],[35],[101]]. Captive
diabetic retinopathy 49594 disturbed.3.2.4. Diabetic RetinopathyThe Nile rat is an exceptional nutritional model for the study of diabetic retinopathy and cataracts, both of which are common in older Nile rats after a prolonged feeding of a hiCHO diet
diabetic retinopathy 49741 which are common in older Nile rats after a prolonged feeding of a hiCHO diet [[34],[100],[101]]. This diabetic retinopathy includes protracted accumulation of leukocytes in retinal arteries when plasma insulin levels are high
glucose intolerance 9013 obesity (DIO). The C57BL/6-DIO mice originally introduced by Surwit et al. (1988) develop obesity, glucose intolerance , moderate insulin resistance, hyperinsulinemia, and increased blood glucose, with fasting glucose levels
glucose intolerance 13711 in adipose tissue is evident. The obesity is accompanied by hyperinsulinemia and hyperglycemia with glucose intolerance [[39],[90]].2.2. Common Rat ModelsAs in mice, high-fat feeding is often applied to conventional inbred
glucose intolerance 14259 for non-obese T2DM. It is an inbred model that spontaneously develops hyperglycemia, glycosuria and glucose intolerance resulting from genetic defects that cause gradual beta-cell degeneration, impaired insulin secretion,
glucose intolerance 14803 in the SDT rat has a polygenic basis, regulated by at least seven quantitative trait loci (QTL) for glucose intolerance : Gisdt1, Gisdt2, and Gisdt3 on rat chromosomes 1, 2 and X and Dmsdt1, Dmsdt2, Dmsdt3 and Dmsdt4 on chromosomes
glucose intolerance 15427 chow (CLEA Rodent Diet CE-2; 63:6:31 CHO:Fat:Protein %energy), male SDT rats exhibited glycosuria and glucose intolerance without obesity at 20 weeks of age. Hyperglycemia, hypoinsulinemia and fibrosis of pancreatic islets
hyperglycemia 2589 adiposity, and fatty liver with increased plasma triglycerides (TG), which lead to rising blood glucose ( hyperglycemia ) and T2DM if sustained [[1],[2]]. It is generally accepted that carbohydrate (CHO), as the dietary glycemic
hyperglycemia 7609 diabetes in homozygous Lepob and Leprdb mice. Both these mouse strains manifest profound obesity, chronic hyperglycemia , and pancreatic beta cell atrophy, resulting in hypoinsulinemia in the C57BLKS/J genetic background.
hyperglycemia 7824 However, in the C57BL/6J genetic background, the same homozygous mutations result in only transient hyperglycemia , and the beta cells undergo hypertrophy (not atrophy), thus resulting in hyperinsulinemia, not true
hyperglycemia 9749 study human MetS because it develops the symptoms of insulin resistance, obesity, hyperinsulinemia, hyperglycemia and hypertension when fed a high-fat diet, it remains lean and physically normal when fed low-fat chow
hyperglycemia 13007 conditions of limited caloric supply. However, the laboratory environment with abundant food results in hyperglycemia in this species, making it a potentially interesting spontaneous model for diet-induced diabetes. However,
hyperglycemia 13692 gain and increase in adipose tissue is evident. The obesity is accompanied by hyperinsulinemia and hyperglycemia with glucose intolerance [[39],[90]].2.2. Common Rat ModelsAs in mice, high-fat feeding is often applied
hyperglycemia 14229 insulin deficiency, especially for non-obese T2DM. It is an inbred model that spontaneously develops hyperglycemia , glycosuria and glucose intolerance resulting from genetic defects that cause gradual beta-cell degeneration,
hyperglycemia 14565 the severe ocular complications of retinal degeneration and detachment associated with the chronic hyperglycemia found in humans with diabetes, rendering this model useful for studying diabetic retinopathy [[73],[74],[75],[76]].Diabetes
hyperglycemia 16280 (18:62:20, 5.04 kcal/g) induced obesity, hyperinsulinemia, and hyperlipidemia between 10 and 16 weeks, but hyperglycemia did not appear until after 16 weeks of age, indicating the hiCHO diet was slightly more diabetogenic.After
hyperglycemia 16465 was slightly more diabetogenic.After 16 weeks of high-fat consumption, the age-dependent progress of hyperglycemia associated with hypoinsulinemia (from insulin deficiency described above) becomes delayed because hyperfunction
hyperglycemia 16700 pancreatic beta cells induced by the high-fat diet appears to suppress development of the hypoinsulinemia/ hyperglycemia . In effect, a high-fat diet improved glucose tolerance and insulin secretion in SDT rats compared to
hyperglycemia 18652 Zucker Diabetic Fatty (ZDF) RatIn the Zucker Diabetic Fatty rat (ZDF), a high-fat diet exaggerates hyperglycemia /hypoinsulinemia and ultimately accelerates the exhaustion of beta cells. While rats did develop diabetes
hyperglycemia 24691 progressive loss of beta cells and spontaneously develops hyperinsulinemia, insulin resistance and hyperglycemia with hyperleptinemia, hyperphagia, increased gluconeogenesis, and accumulation of visceral fat [[70],[71]].The
hyperglycemia 24855 gluconeogenesis, and accumulation of visceral fat [[70],[71]].The β-cell failure is linked to prolonged hyperglycemia /hyperlipidemia, associated with inflammation and oxidative stress. Pathophysiological conditions such
hyperglycemia 25404 confounding effect of high corticosterone, which increases hepatic gluconeogenesis. In fact, their fasting hyperglycemia depends on elevated corticosterone [[72]]. Although increased hepatic gluconeogenesis is a major contributing
hyperglycemia 25546 corticosterone [[72]]. Although increased hepatic gluconeogenesis is a major contributing factor to fasting hyperglycemia in T2DM in humans, it is not associated with increased levels of corticosterone []. Thus, the underlying
hyperglycemia 25674 humans, it is not associated with increased levels of corticosterone []. Thus, the underlying cause of hyperglycemia in the GK rat (and several other rodents) does not closely reflect that in humans and may not be relevant
hyperglycemia 26892 insulin resistance as a consequence of a diet bearing a high glycemic load. This leads eventually to hyperglycemia and insulin deficiency as beta cells fail. The best model of this scenario should adhere to the human
hyperglycemia 28740 stages of insulin resistance with hyperinsulinemia, leading to beta cell failure, and finally to severe hyperglycemia characterized by inadequate insulin production and insulin deficiency associated with ketoacidosis resulting
hyperglycemia 35150 expansion of intra-abdominal fat pools, hypertension, elevated TG with decreased HDL, and eventually hyperglycemia and beta cell failure resulting in depressed insulin and end-stage diabetes that includes severe ketosis
hyperglycemia 49899 leukocytes in retinal arteries when plasma insulin levels are high and pericyte apoptosis, linked to hyperglycemia induced accumulation of Reactive Oxygen Species (ROS), is evident. Han et al. (2017) found that after
hyperglycemia 50175 nicotinamide adenine dinucleotide hydride (NADH) pathway in retinal mitochondrial respiration, but sustained hyperglycemia eventually depressed the NADH pathway in diabetic Nile rats related to an increase in FBG (which in
hyperglycemia 50347 rats related to an increase in FBG (which in itself implies advanced diabetes). Furthermore, increased hyperglycemia was associated with a compromised outer membrane integrity of the mitochondria [[101]].3.2.5. Necropsy
hyperglycemia 50677 nephritis), and cecum enlargement (altered gut flora) corresponding to changes in glucose metabolism and hyperglycemia . Nulliparous hyperglycemic female Nile rats maintained on commercial rat chow for more than a year can
hyperglycemia 53752 dominant gene may interact with environmental (dietary) factors to induce the transition from normo- to hyperglycemia in that model [[47]]. Others have suggested that a cluster of Pdx1 genes affecting insulin secretion
hyperglycemia 63490 between feeding PFJ as a drink or in food [[120]]. Although PFJ rich in polyphenols has proved to reduce hyperglycemia , body weight and T2DM incidence, it tends not to limit the hyperglycemia in the most genetically permissive
hyperglycemia 63563 polyphenols has proved to reduce hyperglycemia, body weight and T2DM incidence, it tends not to limit the hyperglycemia in the most genetically permissive (susceptible) rats that develop the disease on a hiCHO diet (Table
hyperinsulinemia 1460 outcomes. The diabetes is characterized by a striking genetic permissiveness influencing hyperphagia and hyperinsulinemia ; random blood glucose is the best index of disease progression; and kidney failure with chronic morbidity
hyperinsulinemia 2391 onset and progression of these metabolic disorders. MetS is characterized by insulin resistance with hyperinsulinemia , hypertension, depressed high-density lipoprotein (HDL), increased visceral adiposity, and fatty liver
hyperinsulinemia 7911 only transient hyperglycemia, and the beta cells undergo hypertrophy (not atrophy), thus resulting in hyperinsulinemia , not true T2DM. Such models, however, are atypical of the human experience, in part because T2DM in
hyperinsulinemia 9063 introduced by Surwit et al. (1988) develop obesity, glucose intolerance, moderate insulin resistance, hyperinsulinemia , and increased blood glucose, with fasting glucose levels 200 mg/dL [[55]]. Such C57 variants are particularly
hyperinsulinemia 9731 is a good model to study human MetS because it develops the symptoms of insulin resistance, obesity, hyperinsulinemia , hyperglycemia and hypertension when fed a high-fat diet, it remains lean and physically normal when
hyperinsulinemia 13671 however, distinct weight gain and increase in adipose tissue is evident. The obesity is accompanied by hyperinsulinemia and hyperglycemia with glucose intolerance [[39],[90]].2.2. Common Rat ModelsAs in mice, high-fat feeding
hyperinsulinemia 16214 glucose from 12 to 24 weeks. By contrast, a high-fat diet (18:62:20, 5.04 kcal/g) induced obesity, hyperinsulinemia , and hyperlipidemia between 10 and 16 weeks, but hyperglycemia did not appear until after 16 weeks of
hyperinsulinemia 24650 T2DM [[70]]. The model is characterized by progressive loss of beta cells and spontaneously develops hyperinsulinemia , insulin resistance and hyperglycemia with hyperleptinemia, hyperphagia, increased gluconeogenesis,
hyperinsulinemia 26255 mutation (fak) in the leptin receptor. It displays several phenotypes that reflect MetS, such as obesity, hyperinsulinemia , insulin resistance, hyperlipidemia and hypertension [[22],[24],[31],[32]]. However, fasting blood glucose
hyperinsulinemia 28670 captivity and fed chow [[28],[33],[34],[35],[38]]. Both progress through stages of insulin resistance with hyperinsulinemia , leading to beta cell failure, and finally to severe hyperglycemia characterized by inadequate insulin
hyperinsulinemia 35031 into diet-induced T2DM with all the pertinent features of the human condition: insulin resistance, hyperinsulinemia , expansion of intra-abdominal fat pools, hypertension, elevated TG with decreased HDL, and eventually
hyperinsulinemia 62554 stimulate insulin secretion, had no beneficial effect on diabetic Nile rats presumably because the hyperinsulinemia already present does not benefit from further insulin production.The Nile rat has also revealed the
hyperlipidemia 13407 diet. Fed a carbohydrate (sucrose)-rich diet, the spiny mouse develops marked hepatic lipogenesis and hyperlipidemia and elevation of very low-density lipoproteins (VLDL) without obesity or diabetes, although beta-cell
hyperlipidemia 16236 weeks. By contrast, a high-fat diet (18:62:20, 5.04 kcal/g) induced obesity, hyperinsulinemia, and hyperlipidemia between 10 and 16 weeks, but hyperglycemia did not appear until after 16 weeks of age, indicating the
hyperlipidemia 24869 and accumulation of visceral fat [[70],[71]].The β-cell failure is linked to prolonged hyperglycemia/ hyperlipidemia , associated with inflammation and oxidative stress. Pathophysiological conditions such as insulin resistance,
hyperlipidemia 26293 displays several phenotypes that reflect MetS, such as obesity, hyperinsulinemia, insulin resistance, hyperlipidemia and hypertension [[22],[24],[31],[32]]. However, fasting blood glucose is normal, so, despite the several
hyperlipidemia 51953 (BUN) and ketonuria [[33],[35],[104]].Rising RBG and marked elevation in plasma TG and cholesterol ( hyperlipidemia ) (Figure 6A, Table 2) is associated with non-alcoholic fatty liver disease (NAFLD). In severe ketosis,
hyperlipidemia 66777 3Polycystic ovaries in nulliparous 18-month-old female Nile rat fed rat chow. (RBG = 588 mg/dL and severe hyperlipidemia ).Figure 4(A) Kidneys surrounded by Epididymal/Periovarian (Epi) and Peri fat pads; (B) loss of Peri
hypertriglyceridemia 51501 fat, and fatty acids return to the liver to exacerbate hepatic TG formation and secretion resulting in hypertriglyceridemia , and eventually hypercholesterolemia (Table 2).Kidneys often become swollen and enlarged with surface
metabolic syndrome 2131 genetic and molecular mechanisms that characterize human T2DM.1. IntroductionThe current increase in metabolic syndrome (MetS) and type 2 diabetes (T2DM) in the world population emphasizes the urgent need to understand the
obesity 7408 signals. Mutations in the leptin gene (Lep) or its receptor (Lepr) induce hyperphagia, resulting in obesity and diabetes. The genetic background of the strain strongly influences the severity of diabetes in homozygous
obesity 7592 severity of diabetes in homozygous Lepob and Leprdb mice. Both these mouse strains manifest profound obesity , chronic hyperglycemia, and pancreatic beta cell atrophy, resulting in hypoinsulinemia in the C57BLKS/J
obesity 8914 Induced Diabetes in C57BL MouseC57BL/6 mice are among the most sensitive to diet (high-fat)-induced obesity (DIO). The C57BL/6-DIO mice originally introduced by Surwit et al. (1988) develop obesity, glucose intolerance,
obesity 9004 (high-fat)-induced obesity (DIO). The C57BL/6-DIO mice originally introduced by Surwit et al. (1988) develop obesity , glucose intolerance, moderate insulin resistance, hyperinsulinemia, and increased blood glucose, with
obesity 9722 C57BL/6 is a good model to study human MetS because it develops the symptoms of insulin resistance, obesity , hyperinsulinemia, hyperglycemia and hypertension when fed a high-fat diet, it remains lean and physically
obesity 13484 hepatic lipogenesis and hyperlipidemia and elevation of very low-density lipoproteins (VLDL) without obesity or diabetes, although beta-cell hypertrophy is evident. On a fat-rich diet, however, distinct weight
obesity 13645 evident. On a fat-rich diet, however, distinct weight gain and increase in adipose tissue is evident. The obesity is accompanied by hyperinsulinemia and hyperglycemia with glucose intolerance [[39],[90]].2.2. Common
obesity 13885 feeding is often applied to conventional inbred rats, such as the Sprague Dawley strain, to induce obesity and trigger certain aspects of T2DM. In addition, several more specialized models have been described.2.2.1.
obesity 15455 63:6:31 CHO:Fat:Protein %energy), male SDT rats exhibited glycosuria and glucose intolerance without obesity at 20 weeks of age. Hyperglycemia, hypoinsulinemia and fibrosis of pancreatic islets occurred after
obesity 16205 in blood glucose from 12 to 24 weeks. By contrast, a high-fat diet (18:62:20, 5.04 kcal/g) induced obesity , hyperinsulinemia, and hyperlipidemia between 10 and 16 weeks, but hyperglycemia did not appear until
obesity 17046 the complexity of the model. Because insulin resistance and dyslipidemia coexisted with fat-induced obesity , the metabolic response to high-fat intake was concluded to be similar to that observed in other rat
obesity 18324 obese when fed a high-fat diet as the stressor, and high-fat diet is not considered the main cause of obesity and T2DM in humans, the SDT model lacks integrity related both to mode of diet induction and its severe
obesity 19679 Dawley (ZDSD or ZDSD/Pco) RatThe UCD-T2DM and ZDSD rats essentially represent polygenic late-onset obesity with insulin resistance and eventual beta cell insufficiency, while possessing normal leptin signaling.
obesity 20027 2000s by crossing obese insulin-resistant Sprague Dawley (OSD) rats, to provide fat sensitive genes for obesity and insulin resistance, with the Zucker Diabetic Fatty-lean (ZDF fa +/−) rat, to include a genetic
obesity 22763 which dietary macronutrient(s) are responsible for the diet x gene interactions.Furthermore, although obesity and T2DM can develop in both sexes of these newer rat models, female ZDSD rats only do so with a high-fat,
obesity 26246 nonsense mutation (fak) in the leptin receptor. It displays several phenotypes that reflect MetS, such as obesity , hyperinsulinemia, insulin resistance, hyperlipidemia and hypertension [[22],[24],[31],[32]]. However,
obesity 57062 able to better regulate blood sugar, thus making it an attractive therapeutic target for diabetes and obesity , and a good marker of fat storage under stress [[30]]. Chondronikola et al. (2014) found that individuals

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