Pre-insulin treatment of diabetes insipidus,diet food list for diabetes patients,m.i.a twitter - Plans Download

Science, Technology and Medicine open access publisher.Publish, read and share novel research. Non-Obese Type2 Diabetes Animals ModelsYukihito Ishii, Takeshi Ohta and Tomohiko Sasase[1] Japan Tobacco Inc., Central Pharmaceutical Research Institute, Murasaki-cho, Takatsuki, Osaka, Japan1.
Y Goto, K-I Suzuki, M Sasaki, T Ono, S Abe, GK rats as amodel of nonobese, noninsulin-dependent diabetes. Y Goto, M Kakizaki, N Masaki, Spontaneous diabetes produced by selective breeding of normal Wistar rats. Y Tsuura, H Ishida, Y Okamoto, S Kato, K Sakamoto, M Horie, et alGlucose sensitivity of ATP-sensitive K+ channels is impaired in beta-cells of the GK rat. K Ueta, T Ishihara, Y Matsumoto, A Oku, M Nawano, T Fujita, et alLong-term treatment with the Na+-glucose cotransporter inhibitor T-1095 causes sustained improvement in hyperglycemia and prevents diabetic neuropathy in Goto-Kakizaki Rats.
H Yamamoto, Y Uchigata, H Okamoto, Streptozotocin and alloxan induce DNA strand breaks and poly(ADP-ribose) synthetase in pancreatic islets. M Kergoat, B Portha, In vivo hepatic and peripheral insulin sensitivity in rats with non-insulin-dependent diabetes induced by streptozocin. Acanthosis Nigricans is a skin disorder that makes the folds of the skin thicker, darker and velvety. Though the disorder can strike a person of any gender, descent and age, it is more common in people of African origin.
The symptoms of Acanthosis Nigricans mainly consist of the skin turning darker and more velvety. Lymphoma or cancerous conditions of the genitourinary or gastrointestinal tracts can also result in Acanthosis Nigricans.
Use of medicines like contraceptive pills and human growth hormones can also lead to this disease. Acanthosis Nigricans can be diagnosed by an expert medical professional by mere physical observation. Acanthosis Nigricans generally disappears after a few days without the need of any treatment. If obesity is found to be a cause, the affected person may have to take up daily exercise to lose weight fast. When Acanthosis Nigricans affects people older than 40 years, it usually results from an internal malignancy or Adenocarcinoma of the uterus or Gastrointestinal tract.
Mild cases of can be treated using a Glucocorticoid Acanthosis Nigricans cream like Panolog. If you are having Acanthosis Nigricans cases in your family or suffering from the disease yourself, it is best to wait for a week or two.
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Use the form below to delete this Trigger Finger Home Remedies Natural Treatments And Cure image from our index. Use the form below to delete this From Obesity Diabetes Alcoholism Malnutrition To Drug Induced image from our index. In a groundbreaking study in 2011 on reversal of type 2 diabetes, researchers at Newcastle University in England put 11 people diagnosed with diabetes within the previous four years through a carefully planned, extreme 600 kcal-a-day diet for eight weeks. The study, published in Diabetologia, dramatically reaffirmed the well-known fact that type 2 diabetes can be effectively managed or cured through lifestyle management.
The corollary to this, of course, is that certain foods, when added to your daily diet, can certainly help prevent diabetes. Unsalted almonds are a good source of monounsaturated fats and low in carbs, while being rich in magnesium, which is believed to be important for carbohydrate metabolism.
Add in your diet: The flavour of almonds goes up manifold when they are dry-roasted in the oven.
While wholegrains have been proven to prevent diabetes, they lower average blood sugar and insulin levels, and improve cholesterol and triglyceride levels in those who already have type 2 diabetes. Making a sudden transition from refined foods like white flour to wholegrains can lead to a bloated and uncomfortable feeling, so make it gradual. Add in your diet: Have three-four cups of lightly brewed black or green tea, with minimal milk and no sugar, for maximum benefits.
I will show you an easy and safe way to assess how far down the Road to Diabetes you have already travelled. The following test is my version of the Glucose Tolerance Test which is used by doctors to determine if you are diabetic or not. If you discover you are diabetic, you should continue to take another glucose test every hour, for another four hours, or until glucose drops below 105. According to me, there is a right way and a wrong way to eat to avoid or slow down diabetes.
Fortunately, I think that now I have finally learned to eat correctly because now I learned to test my glucose levels before and after most meals.
How far down that road to diabetes we have already travelled depends on the state of our pancreas, and very few people know how well their pancreas is working.
The values obtained tell a lot about your body metabolizes sugar, and the state of the pancreas. FOUR ENGINES-- You are flying high and fast, Clear weather ahead, no problems are expected.
However, now that you know that you have lost one engine it makes sense that you should do everything possible to avoid losing any other engine, which would definitely not be good for your health.
Severe symptoms, including psychotic or neurotic behaviour, might occur during the traditional glucose tolerance test, but probably not with a large glass of orange juice. No part of this site or its content may be reproduced in any form or by electronic or mechanical means, including information storage and retrieval systems, without permission in writing from the copyright holder.
The information provided on this site is provided for illustration purposes only and does not represent a proposal or specific recommendation. Effect of DPPIV-i on blood glucose (A) and insulin (B) levels in glucose-loaded SDT fatty rats. IntroductionDiabetes mellitus has become a global health problem, and the incidence of the disease is increasing rapidly in all regions of the world. H Giroix, B Portha, M Kergoat, D Bailbe, L Picon, Glucose insensitivity and amino-acid hypersensitivity of insulin release in rats with non-insulin-dependent diabetes.
In rare cases, other areas of the body such as palms, lips and soles of the feet may also be affected.
Excess insulin results in production of melanocytes, cells that are the cause of pigmentation in humans.
Many obese people suffer from diabetes and endocrine disorders which can trigger Acanthosis Nigricans.
However, skin biopsies, X-Rays and endoscopy may be recommended if the doctor suspects diabetes or any cancerous condition to be the cause. However, persistent symptoms of the disease call for an effective Acanthosis Nigricans cure. For obese people with diabetes Acanthosis Nigricans recovery can be faster with rapid loss of weight. Obese people are frequently seen to suffer from Insulin Resistance, which arises due to Type 2 Diabetes or Pre-Diabetes. Adenocarcinoma can also affect other regions of the body such as breast, prostate gland, stomach, ovary or lung. This is basically a corticosteroid cream which has antibacterial, antifungal and anti-inflammatory properties.
Unsalted roasted almonds can be chopped and added to salads, or eaten as it is for a snack. Another study published in the same journal establishes that consuming cheese or yogurt may help prevent diabetes. These also have anti-inflammatory, hypolipidemic (decreasing lipid levels) and blood sugar-reducing properties.
But now that you know that you are in trouble, you should take very good care of your two remaining engines so that you won't lose another one!
As a word of caution, the information presented cannot possibly substitute for competent medical advice.
A high insulin level can result from a number of disorders like pre-diabetes, diabetes and insulin resistance.
Check out these Acanthosis Nigricans images and see whether the patches on your skin are similar to the ones shown here. In such situations, Acanthosis Nigricans can be a sign of life-threatening conditions in the body. Acanthosis Nigricans of the tongue or mucous membrane of the mouth is usually a sign of a tumor in the Gastrointestinal Tract.
The disease mainly arises in canines due to Hypothyroidism, Hormonal imbalance, Food allergies and obesity.
These foods give an extra boost to a healthy diet—they have been shown not only to help stabilize blood sugar and prevent diabetes, but if consumed regularly, also help in weight management, reduce the risk of cardiovascular diseases, help prevent bowel cancers, keep bones and muscles in better shape, and more. The study involved 65 pre-diabetic adults who were divided into two groups to determine the effect of almond consumption.
Scientists believe that the fermentation process that converts milk to cheese and yogurt could be responsible for their anti-diabetic property. However, tea is best had brewed lightly and with minimal milk, rather than the overtly sugary boiled-over-several-minutes traditional beverage preferred by most Indians.
The seeds contain an amino acid not found in mammalian tissues, 4-hydroxyisoleucine, which is supposed to increase insulin production by stimulating those cells of the pancreas that secrete insulin. Cinnamon has an inherent sweetness that works on satisfying the sweet tooth just like sugar does, helping to reduce sugar consumption.

King, Indiana University School of Medicine and Indiana University Center for Regenerative Biology and Medicine, Terre Haute, IN.
The glucose and the insulin levels were examined at immediately before glucose-loading, 30, 60, and 120 min after glucose-loading. The glucose (A) and the insulin (B) levels were examined at immediately before glucose-loading, 30, 60, and 120 min after glucose-loading. For example, prevalence of diabetes across the world is forecast to increase from 171 million in 2000 to 366 million in 2030 [1].Diabetes mellitus is classified into two categories, type 1 and type 2. Read on to know all about Acanthosis Nigricans, its causes, symptoms, diagnosis and treatment.
Obese kids are also at a higher risk of developing Type 2 diabetes some years later in their lives. Three months after the end of the diet, even though the patients had returned to eating normal (but healthy) food, seven of them had been cured completely. One group ate a healthy diabetic diet without nuts and the other group ate the same diet, but with 20% of the calories from almonds (roughly 2 ounces [around 55g] per day). The probiotic bacteria in yogurt lowers cholesterol and produces certain vitamins that help prevent diabetes.
The one drawback is the bitter taste, which can be masked when added to food preparations instead of eating them as it is.
In order to arrive to your destination it will be very important to care for your last remaining engine.
Type 1 diabetes mellitus (T1D or IDDM; Insulin Dependent Diabetes Mellitus) is characterized by a loss of insulin secretion due to pancreatic ?-cell degeneration, leading to autoimmune attack.
Dietary modifications can help both Acanthosis Nigricans children and adults recover within a month.
Analysis showed that the group that ate almonds had much better insulin levels and improved markers of beta-cell function. Dairy products like cheese, milk and yogurt are also rich in vitamin D, calcium and magnesium, which may help protect against the condition. They found that across 50 countries, places where people drink black tea more, people had significantly lower rates of type 2 diabetes. It is possible that the flavonoids help to regenerate the insulin-secreting cells in the pancreas. If you have a particular question about the information presented, you can send me an e-mail and I will try my best to help you. Development of T2D is usually caused by several factors, which are combined with lifestyle, genetic defects, virus infection, and drugs [3, 4].
Sustained hyperglycemia causes severe diabetic microvascular complications, such as retinopathy, peripheral neuropathy, and nephropathy. In the diabetic states, multiple mechanisms have been implicated in glucose-mediated vascular damage and contribute to diabetic microvascular complications. In addition, postprandial state is also an important factor in the development of macroangiopathy. In diabetes, the postprandial phase is characterized by an exaggerated rise in blood glucose levels. It has recently been shown that postprandial hyperglycemia is relevant to onset of cardiovascular complications. From this evidence, treatment of diabetes has become a part of the strategies for the prevention of diabetic vascular complications.To help develop new diabetic treatments, it is important to reveal the complex mechanisms of diabetes.
In particular, studies using diabetic animal models are essential to aid in clarification of the pathogenesis and progression in human disease course.
In this chapter, we review these three types of T2D animal models with respect to characteristic features, including impaired glucose tolerance.2. Non-obese type 2 diabetic animal modelsCertain non-obese diabetic models are used in the investigation of T2D in humans.
Since the GK rat is generally considered as one of the best models of T2D, many researchers have used this animal model to study the physiology of diabetes and its complications, and to evaluate anti-diabetes drugs. In 1973, Goto and Kakizaki of Tohoku University (Japan) started selection of this substrain from Wistar rats by mating pairs with glucose intolerance.
Since F8, sister-brother mating has been repeated, and were established as an SPF animal at F29.
Today, many colonies of the GK rat exist and the rats are available for purchase from several breeders.The major quantitative trait locus (QTL) for impaired glucose tolerance is Niddm1, identified in chromosome 1. Several loci linked to pathophysiologic characteristics was observed on chromosomes 2, 4, 5, 8, 10, and 17, indicating that the diabetic features in GK rats are inherited as polygenic traits and that GK rats would provide insights into genetics of human T2D [7]. Glucose tolerance and insulin sensitivityNon-fasting blood insulin levels in GK rats are slightly higher than in age-matched Wistar rats. Impaired glucose-stimulated insulin secretion has been reported in GK rat in vivo [8], in the isolated pancreas [9], and in isolated pancreatic islets [10]. Perfusion experiments using isolated pancreas showed that the first phase of insulin secretion by glucose stimulation was impaired in GK rats, although the response to arginine was preserved [9].“Starfish-shaped” islets are a morphological feature of GK rat. The number of enlarged islets with irregular shape, ill-defined borders, and fibrous strands of endocrine cells is increased in aged GK rats.
These islets showed similar or moderately decreased insulin content compared with control rats. Pancreatic glucagon content is at almost the same level as in Wistar rats, and somatostatin content is slightly higher in GK rats [11].
The defective insulin response to glucose in ?-cells is due to abnormalities in the function of K+ATP channels and L-type Ca2+ channels [12].The GK rats show mild insulin resistance, mainly considered to be due to increased hepatic glucose production [8]. Drug treatment and diabetic complicationsGK rats have been widely used for evaluating anti-diabetic drugs.
Almost all types of such drugs have been tested with GK rats, including sulfonylureas [13], an ?-glucosidase inhibitor [14], a thiazolidinedione derivative (troglitazone) [15], a biguanide (metformin) and a gluconeogenesis inhibitor [16], a GLP-1 analog and a dipeptidyl peptidase-4 inhibitor (DPPIV-i) [17], and an SGLT2 inhibitor [18].In addition to its useful features as a T2D model, GK rat has been used as model of diabetic complications. Reduced motor nerve conduction velocity (MNCV) in the caudal nerve is reported in 2-month-old GK rats [19].
BackgroundStreptozotocin (STZ) is an antibiotic derived from Streptomyces achromogenes that has selective toxicity to pancreatic ?-cells.
STZ induces DNA strand breaks and a consequent excess activation of poly (ADP-ribose) synthetase, an enzyme that repairs DNA, depleting NAD in cells, which leads to energy depletion and finally causes ?-cell death [22]. Neonatal rats treated with STZ at birth (nSTZ rat) revealed acute insulin deficient diabetes at 3-5 days after birth [23]. Their pancreatic insulin contents reduced to 7% that of normal rats, and showed hyperglycemia in this period. However, after this period, blood glucose and insulin levels in nSTZ rats were almost the same as in control rats at 3 weeks of age. At eight weeks of age, nSTZ rats showed mild hyperglycemia and impaired glucose tolerance with a 50% decrease in pancreatic insulin content [24].Recently, Masiello et al.
When given a calorie-controlled high fat diet, hyperlipidemia and insulin resistance without obesity were observed [26].
Glucose toleranceThe reduction of ?-cell number and insulin content in the pancreas leads to defective insulin response in vivo. An isolated pancreas perfusion study using adult nSTZ rats showed lack of insulin response to glucose stimulation, indicating loss of ?-cell function [27]. Reduction of GLUT2 expression in ?-cells may attribute to impaired glucose entry into ?-cells and the following insulin secretion [28]. Reduced sensitivity of KATP channel to extracellular glucose has also been suggested by the patch-clamp technique [29].
Furthermore, an in vivo study has indicated that the hepatic glucose production (HGP) in the basal state is higher in adult nSTZ rats than in control animals [30].
Ghrelin, the hunger-stimulating peptide produced in stomach, also promotes regeneration of ?-cells in nSTZ rats.
Treatment with ghrelin increased pancreatic expression of insulin and Pdx1 mRNA with a consequent improvement of hyperglycemia in nSTZ rats [38].3.
Obese type 2 diabetes animal modelsObesity is a well-established risk factor for many chronic disorders, such as T2D [39].
To understand the complicated features of the disease, spontaneously T2D models provide important knowledge.
In particular, the development of diabetic animal models and pathophysiological analyses of the models are very important to aid in clarification of the pathogenesis and the patterns of progression in the human disease course. BackgroundZucker diabetic fatty (ZDF) rat is an obese animal associated with hyperphagia, hyperglycemia, hyperinsulinemia, and hyperlipidemia. Insulin resistance is caused by age-dependent degeneration in pancreatic ?-cells that trigger hyperglycemia. Thus, ZDF rat is a widely studied model of obesity and insulin resistance and is used for evaluation of anti-diabetic drugs.
ZDF rat was discovered in a colony of outbred Zucker fatty (ZF) rat in the laboratory of Dr. Richard Peterson at Indiana University Medical School (IUMS) started selection of this rederivation, and established an inbred line of ZDF rat in 1985. It is well known that sexual differences exist in the incidence and progression of diabetes mellitus in ZDF rat [41]. Diabetes mellitus has developed in more 90% of the males, whereas the blood glucose level remains normal in most females. However, female ZDF rat became diabetic on high-fat diet, and it was shown that the dietary fat content affected development of diabetes in females [41]. Glucose tolerance and insulin sensitivitySerum glucose levels in ZDF rat are usually elevated from 7-10 weeks of age. ZDF rats showed hyperinsulinemia from 6 to 12 weeks, but after about 14 weeks of age their insulin levels showed a tendency to decrease.
Glucose intolerance at 12 weeks becomes more severe than that at 5-7 weeks of age [42, 43]. Age-dependent degenerative changes of pancreatic islets showed decreased production and secretion of insulin, and atrophy of islets.
Early pathological changes of the pancreatic islets, such as hypertrophy, disarray of islet architecture, and irregular islet boundaries, were observed by 10-12 weeks of age [44, 45]. The specific factor that causes deterioration of pancreatic ?-cells has not been identified, but changes in ?-cell structure and function have been well studied. It was reported that lipotoxicity based on high plasma free fatty acid could attribute to ?-cell dysfunction [46]. Reduction of islet mRNAs in ?-cells, such as those for insulin, GLUT2, and glucokinase, contributes to the ?-cell deterioration [42].
Furthermore, decrease in GLUT4 expression is also observed in skeletal muscle and adipose tissue of ZDF rat [47]. Drug treatment and diabetic complicationsIt is well known that ZDF rat is a useful model for evaluating anti-diabetic compounds.
Other compounds also have been evaluated in ZDF rat, including a sulfonylurea [48], ?-glucosidase inhibitors [49], a thiazolidinedione (pioglitazone) [50], a biguanide (metformin) [51], a GLP-1 analog [52], an SGLT2 inhibitor [53], a ?3-andrenergic receptor agonist [54], and a variety of other compounds [55-58].A number of studies demonstrated that ZDF rat can be used as model of diabetic complications. Blood urea nitrogen (BUN) levels and urinary protein excretion in ZDF rat were elevated from about 40-50 weeks of age.

Reduced MNCV in the sciatic nerve is observed from 12–14 weeks of age in ZDF rats, and endoneurial blood flow (EBF) in the sciatic nerve is also decreased after 24 weeks of age [60]. The degeneration and swelling of fibrae lentis, formation of Morgagnian globules, and stratification of epithelium lentis cells is observed in ZDF rat at 21 weeks of age [61, 62].
BackgroundOtsuka-Long-Evans-Tokushima-Fatty (OLETF) rat is a mildly obese animal associated with polydipsia, polyuria, polyphagia, hyperglycemia, and hyperlipidemia. OLETF rat is considered to be a suitable model for understanding the properties of T2D with mild obesity. The spontaneously obese rat with T2D was obtained from a colony of outbred Long-Evans rat, available for purchase from Charles River, in 1984 at laboratory of Otsuka pharmaceuticals, Tokushima [63]. A strain of this rat was established by sister-brother mating with obesity and glucose intolerance. According to the results of a study by Takiguchi [64, 65], a disrupted cholecystokinin-A (CCK-A) receptor gene in peripheral tissues and central nervous system is found in the OLETF rats [64].
Meanwhile, in peripheral tissues, CCK-A also controls satiety signals through the vagal afferent neurons [67].
Thus, dysfunctional signal of CCK may cause obese T2D, leading to hyperphagia in OLETF rats. Glucose tolerance and insulin sensitivityNon-fasting plasma glucose levels in OLETF rats were elevated from 18 weeks of age, and the increase was sustained until 40 weeks of age.
Diabetes mellitus developed in about 90% of OLETF rats at 30 weeks of age, whereas the plasma glucose level remained normal in most females at 24 weeks of age [63, 68]. Sexual differences exit in the incidence and progression of diabetes mellitus in OLETF rats [69]. In glucose tolerance test, marked elevation of plasma glucose and insulin level responses to glucose are observed at 24 weeks of age [63]. Age-dependent degenerative changes of pancreatic islets are observed from 16 weeks of age [70]. The pathological changes of the pancreatic islets, such as hypertrophy, atrophy of insulin positive-?-cells, fibrosis, and indistinct, irregular islet boundaries, were observed by 30 weeks of age [71]. These dysfunctions of ?-cells seem to cause the development of glucose intolerance in OLETF rats. Insulin resistance has been reported in OLETF rats at 16 weeks of age, as measured by hyperinsulinemic euglycemic clamp technique [70]. In adipocytes, the GLUT4 protein expression considerably decreased in OLETF rats at 30 weeks of age.
The decrease in GLUT4 protein in muscles is also observed in OLETF rats at 30 weeks of age [72]. Drug treatment and diabetic complicationsOLETF rats have been widely used for pharmacological evaluation while testing for many anti-diabetic drugs, including a Ca2+ antagonist [73], sulfonylureas [74], an ?-glucosidase inhibitor [75], a thiazolidinedione [76], a biguanide (metformin) and a gluconeogenesis inhibitor [77], and a GLP-1 analog [78].OLETF rats are also used as a model for assessment of diabetic complications.
It was reported that histopathological changes in the kidney were observed after 23 weeks of age. OLETF rats at 55 weeks of age showed an expansion of the mesangial matrix and aneurismal dilatation of intraglomerular vessels [63]. It is known that lenticular sorbitol level increases in OLETF rats from 40 weeks of age [79].
OLETF rats show swelling and liquefaction of lens fibers in the subcapsular and supranuclear region at 60 weeks of age. BackgroundWistar fatty rat develops obesity with hyperphagia, hyperglycemia, hyperinsulinemia, hyperlipidemia, and glucose intolerance. Wistar fatty rat is a good model for studying obesity and insulin resistance, and for evaluation of anti-diabetic drugs. Wistar fatty rat was established as a congenic line of the insulin resistance of the Wistar Kyoto strain (WKY) rat by introducing the fa allele of the ZF rat for obesity into the WKY rat genome in the laboratory of Dr. At 5th generation of backcrossing, male obese animals exhibit hyperglycemia, and were established as Wistar fatty rat at 10th generation.
Glucose tolerance and insulin sensitivityNonfasting plasma glucose levels in Wistar fatty rats were elevated until 8 weeks of age, and this level was sustained until 24 weeks of age.
Wistar fatty rat is a widely studied model used to investigate the pathogenesis of obesity and insulin resistance, and for evaluation of anti-diabetic drugs.
In glucose tolerance test conducted at 12 weeks of age, Wistar fatty rat showed higher serum glucose and insulin levels after glucose loading compared with WKY rat, and glucose intolerance became more severe age-dependently. Hypertrophied pancreatic islets in Wistar fatty rat were increased in pancreas compared with WKY rat [80].
Insulin resistance has been reported in Wistar fatty rats, confirmed by glucose clamp technique [82]. Decreased insulin-stimulated glycogen synthesis and glycolysis in the isolated soleus muscles, and insulin-stimulated glucose oxidation and lipogenesis in adipocytes were observed in Wistar fatty rats [83].
Drug treatment and diabetic complicationsWistar fatty rats have been used as a good model for evaluation of a number of anti-diabetic drugs, including a biguanide [84], an ?-glucosidase inhibitor [75], a thiazolidinedione [85], and an DPPIV-i [86].Wistar fatty rats are also used as a model of diabetic complications.
It was reported that age-related increases in urinary NAG (N-acetyl-beta-D-glucosaminidase) and urinary protein and albumin excretion in Wistar fatty rat were elevated from 5-11 weeks of age. Wistar fatty rats at 26 weeks of age showed an expansion of the glomerular mesangial matrix and local formation of a nodular-like lesion. Reduced MNCV in the fibula nerve and histopathological changes, such as demyelination and axonal degeneration, were observed in Wistar fatty rats [88].
BackgroundThe Spontaneously Diabetic Torii (SDT) rat is a new inbred strain of Sprague-Dawley (SD) rat established as a non-obese model of type 2 diabetes mellitus. The cumulative incidence of diabetes was 100% by 32 weeks in male SDT rats, while it was only 33% in females even at 65 weeks. As a result of chronic severe hyperglycemia, the SDT rats developed severe complications in eyes, peripheral nerves, and kidneys. Especially, ocular complications including the diabetic retinopathy in SDT rats is noteworthy [90]. Of many diabetic ocular complications, cataract, retinopathy, and neovascular glaucoma (hemorrhagic glaucoma) are the most important clinically. Glucose tolerance and insulin sensitivityIn SDT rats, development of hyperglycemia may be more dependent on decreased insulin secretion than insulin resistance, as shown by the fact that the blood insulin concentration tended to be lower than in normal SD rats even before the onset of diabetes, and marked hypoinsulinemia developed after the onset of hyperglycemia [91-93], indicating that this strain of rat is a model of non-obese T2D associated with impaired insulin secretion. In oral glucose tolerance test in SDT rats, glucose tolerance markedly decreased at least 3 months before manifestation of hyperglycemia (around 16 weeks old), and the rate of rise in blood glucose level after glucose-loading increased with age. We examined the glucose tolerance periodically at 5, 9, and 13 weeks of age in SDT rats (Figure 1.). Figure 1.Glucose tolerance test (GTT) at 5, 9, and 13 weeks of age in SD rats and SDT rats. The blood glucose level before glucose-loading and the level at 120 min after glucose-loading in SDT rats significantly decreased as compared with those in SD rats. The blood insulin level at 30 min after glucose-loading was not different from that in SD rats, but the insulin levels at the other points significantly decreased as compared with those in SD rats (Figure 1B.). The insulin levels at points except for 120 min after glucose-loading in SDT rats was comparable with those in SD rats (Figure 1D.), but the insulinogenic index showed a lower level than SD rats (Figure. In male rats, the severity of impaired glucose tolerance before the onset of diabetes was closely correlated with the age.
In addition, the insulin secretion level in pancreatic islets of Langerhans from SDT rats after glucose treatment markedly decreased at 12 weeks of age and thereafter compared with normal SD rats.
Likewise, the mRNA expression levels for GLUT2 and glucokinase (GK) in the isolated pancreatic islets of Langerhans markedly decreased at 12 weeks and thereafter in SDT rats [94]. In female rats, glucose tolerance also decreased, at 25 weeks and thereafter, but insulin was secreted after glucose-loading, indicating that some factors cause insulin resistance or insulin requirement in the females, unlike in the males [95].It is reported that the pancreatic insulin content in SDT rats at 7 weeks of age decreased as compared with that in SD rats [96]. In human, ? cell mass in impaired fasting glucose (IFG) subjects significantly decreased as compared with that in nondiabetic subjects [97]. Other non-obese type 2 diabetic models, such as GK rats and the nSTZ rats, did not show a pre-diabetic state. Drug treatmentIn previous study, ?-glucosidase inhibitor voglibose was administered to male SDT rats in a pre-diabetic stage, and the effects of voglibose on the glucose intolerance and the development of diabetes were investigated [98]. Moreover, voglibose was administered as a dietary mixture to SDT rats from 10 to 20 weeks of age. In clinical study, ?-glucosidase inhibitor, such as voglibose and acarbose, showed a prevention of type 2 diabetes mellitus [99, 100]. The results showed that pharmacological intervention with voglibose in SDT rats with IGT can delay progression to T2D.
The decreased sensitivity to insulin leads to an increased requirement for insulin, and is often associated with obesity in which metabolic disturbances are marked in insulin-target organs, such as the liver, muscle and adipose tissues [102].
Obesity plays key roles in the pathophysiology of several metabolic diseases and is a risk factor for diabetes mellitus and dyslipidemia. Based on the above concept, a novel model of obesity-related diabetes was established by Masuyama et al.
They established a congenic line of the Spontaneously Diabetic Torii (SDT) rat by introducing the fa allele of the ZF rat into the SDT rat genome via the Speed Congenic Method using a PCR technique with DNA markers. This congenic strain has been maintained by inter-crossing between fa-heterozygous littermates. Glucose tolerance, insulin sensitivity and drug treatmentMetabolic disorder in SDT fatty rats was obviously promoted as compared with SDT rats [104, 105]. Serum glucose levels in SDT fatty rats of both sexes were elevated from 6 weeks, and lipid parameters such as serum triglyceride and total cholesterol levels in the rats were elevated from 4 weeks of age. With early incidence of diabetes mellitus, diabetes-associated complications in SDT fatty rats were seen at younger ages than those in the SDT rats. SDT fatty rats did not almost show a pre-diabetic state, since the rats showed a hyperglycemia from a young age.
However, the glucose intolerance in SDT fatty rats is considered to exist with the progression of diabetes mellitus.We evaluated the pharmacological effects of an anti-diabetic drug, DPPIV-i on SDT fatty rats. DPPIV-i is expected to control postprandial hyperglycemia in patients with type 2 diabetes mellitus without increasing body weight.
SDT fatty rats at 9 weeks of age showed a prominent hyperglycemia after glucose-loading (Figure 4A.).
The glucose levels at 30 and 60 min after glucose-loading in the SDT fatty rats significantly increased as compared with those in SD rats.
Moreover, the insulin levels at 30 and 120 min after glucose-loading in the SDT fatty rats increased as compared with those in SD rats (Figure 4B.).
The GSIS in SDT fatty rats was accelerated as compared with SD rats, suggesting that hyperinsulinemia (insulin resistance) exists in the SDT fatty rats at 9 weeks of age. Glucose intolerance in SDT fatty rats is considered to be related with both the insulin resistance and the impaired insulin secretion. Each of these models has different features as described above (Table 1.), and each model acts as an important tool for revealing the complex mechanisms of diabetes and developing new anti-diabetic drugs. Studies using diabetic animal models are especially essential to aid in clarification of the pathogenetic development in human T2D.

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