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The TSOD mouse has been established as an inbred strain with spontaneous development of diabetes mellitus as the first clinical signs of diabetes. Polydipsia and polyuria are observed at about 2 months old only in male mice, after which hyperglycemia and hyperinsulinemia are detected. Following these symptoms obesity gradually develops until about 12 months old. In histopathological examination of the pancreas, severe hypertrophy of pancreatic islets was observed due to proliferation and swelling of B cells. In the kidney, thickening of the basement membrane in glomeruli and an increase of the mesangial area were observed at 18 months old. Motor neuropathy in TSOD mice began to appear at 14 months old and most male mice at 17 months old showed weakness of front and hind paws caused by neuron degeneration in the peripheral nerve. In sensory neuropathy, the threshold in the tail pressure test decreased significantly at 12 months old. Light microscopic and electron microscopic examination of sciatic nerves showed a decrease in the density of nerve fibers by the endoneural fibrosis and loss of these fibers. Degenerative changes of myelinated fibers, separation of myelin sheaths with intralamellar edema and remyelination were frequently observed. In the severely affected nerve fibers, the lamellar structure was completely destroyed and macrophages migrated around the myelin sheath or invaded the intramyelin space. Considering these findings similar to non-insulin dependent diabetes mellitus (NIDDM) in humans, the TSOD mouse should be a useful model for the pathogenic study of diabetic complications, especially of peripheral neuropathy.
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PMID:Diabetic complications in a new animal model (TSOD mouse) of spontaneous NIDDM with obesity. 1572 83

An adrenal tumour was diagnosed in a 12-year-old female cross-bred terrier. The dog was presented to the veterinary clinic because she had been gaining weight and had started urinating in the owners' house. Clinical findings included obesity, abdominal enlargement, thinning of the hair coat, seborrhoea sicca, and polydipsia and polyuria. The diagnosis was made by clinical pathology, endocrine function tests and abdominal radiography. Surgical removal of the neoplastic right adrenal gland resulted in resolution of the clinical signs, including regrowth of the hair coat.
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PMID:Adrenal adenoma in a cross-bred terrier. 1603 24

Hyperadrenocorticism is a common endocrinopathy which results from the excessive production of cortisol by the adrenal cortex. In the majority of cases, this increased secretion of cortisol results from stimulation of the adrenal cortex by adrenocorticotrophic hormone secreted from the pituitary gland. In a smaller number of cases adrenal tumours are present. Clinical signs are variable but commonly include polydipsia and polyuria, polyphagia, obesity, a pendulous abdomen, hepatomegaly, alopecia, lethargy, weakness and anoestrus. Haematology, serum chemistry analysis and urinalysis should be performed on a dog with suspected hyperadrenocorticism. Finding a significant number of changes that are consistent with hyperadrenocorticism often allows a presumptive diagnosis to be made. Other tests can then be used to confirm the diagnosis and to help localise the cause, including liver biopsy, radiology, ultrasonography, gamma camera imaging, computed tomography, and measurement of blood and urine hormone levels. The ACTH stimulation test, low dose dexamethasone suppression test and measurement of the urine cortisol:creatinine ratio are used to assess whether hyperadrenocorticism is present. The high dose dexamethasone suppression test, measurement of plasma ACTH, corticotropin-releasing hormone stimulation test, and a modification of the urinary cortisol:creatinine ratio test are then implemented to determine the aetiology. The treatment of choice for adrenal neoplasia is surgical removal of the affected adrenal. On the other hand, pituitary hyperplasia or neoplasia may be treated either surgically, by bilateral adrenalectomy or hypophysectomy, or medically. The drug which is chosen most commonly for medical management is 1,1-dichloro-2(O-chlorophenyl)-2-(P-chlorophenyl) ethane (op'-DDD), which can be used to suppress adrenal function or to completely destroy the adrenal cortex. The antifungal agent ketoconazole also suppresses adrenal steroid synthesis and provides an alternative form of medical treatment for hyperadrenocorticoid dogs.
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PMID:Canine hyperadrenocorticism. 1603 96

The increasing prevalence of type 2 diabetes in the USA has closely paralleled the increase in childhood obesity noted there, but now across the Western world and therefore in Belgium. (Pre)type 2 diabetes is preceded by insulin resistance which must be diagnosed and treated. In Belgium, type 1 diabetes is the predominant (97%) form of diabetes in young people (< 2,000 cases under the age of 18 years). Type 1 diabetes is an auto-immune disease which is more aggressive in younger children. At onset, the key-symptoms are : polyuria, polydipsia, weight loss, asthenia. Diagnosis is confirmed with 2 strips measuring glycaemia and glycosuria. Treatment and diabetes education for self-management should be initiated immediately in paediatric clinics of diabetology with a specialised multidisciplinary team. Thanks to the Belgian Social medicine, medical consultations and material necessary for treatment are nearly without cost. The principal aims of therapeutic management of the child, adolescent and adult with type 1 diabetes are to allow good quality of life and to avoid long-term complications by maintaining blood glucose concentrations close to the normal range and an HbA1c level under 7%. The number of daily insulin injections, 2 or > or = 4, by itself does not necessarily give better results, but the 4-injection regimen allows greater freedom, taking into account that the proper insulin adjustment is difficult before adolescence. Successful glycaemic control in young patients depends mainly on the quality and intensity of diabetes education. Any dogmatism must be avoided. Dietary recommendations issued over the last few years are the same for diabetic and non-diabetic individuals in order to avoid degenerative diseases. In the twice-daily injection regimen, the allocation of carbohydrates throughout the day is essential. Due to their pharmakokinetic characteristics, rapid-acting and long-acting insulin analogues have specific indications in both the twice-daily injection regimen and the basal-bolus insulin therapy. They improve quality of life, without necessarily reducing HbA1c.
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PMID:[Management of children and adolescents with diabetes mellitus: personal experience]. 1624 Aug 70

Hummingbirds and other nectar-feeding, migratory birds possess unusual adaptive traits that offer important lessons concerning obesity, diabetes and the metabolic syndrome. Hummingbirds consume a high sugar diet and have fasting glucose levels that would be severely hyperglycemic in humans, yet these nectar-fed birds recover most glucose that is filtered into the urine. Hummingbirds accumulate over 40% body fat shortly before migrations in the spring and autumn. Despite hyperglycemia and seasonally elevated body fat, the birds are not known to become diabetic in the sense of developing polyuria (glucosuria), polydipsia and polyphagia. The tiny (3-4 g) Ruby-throated hummingbird has among the highest mass-specific metabolic rates known, and loses most of its stored fat in 20 h by flying up to 600 miles across the Gulf of Mexico. During the breeding season, it becomes lean and maintains an extremely accurate energy balance. In addition, hummingbirds can quickly enter torpor and reduce resting metabolic rates by 10-fold. Thus, hummingbirds are wonderful examples of the adaptive nature of fat tissue, and may offer lessons concerning prevention of metabolic syndrome in humans.
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PMID:Adipose energy stores, physical work, and the metabolic syndrome: lessons from hummingbirds. 1635 26

Prevalence of type 2 diabetes (T2DM) in children and adolescents has increased, parallelled to the increased prevalence of obesity around the world. The objectives of this study are (1) to identify the clinical presenting features of T2DM in Thai children and adolescents, and (2) to identify evidence of feature of metabolic syndrome in these affected. We analyzed 26 T2DM patients who were treated by Pediatric endocrinologists in our hospital. The study showed that their mean ages (+/- SD) at diagnosis was 12.1 +/- 2.3 years, all were obese and 96% had acanthosis nigricans. Fifty three percents (53%) presented with clinical signs and symptoms which included DKA (19.2%), clinical triad of polyuria, polydipsia and weight loss (15.4%), only polyuria, polydipsia (11.5%) and abnormal menstruation (7%). The rest of 46.2% had no clinical symptoms. The initial fasting or random plasma glucose found above diagnostic range in 84.5%, the rest of 15.5% were diagnosed by using oral glucose tolerance test. Dyslipidemia was found in 75%. Fifteen percents had no family history. Eighty percents had three or more than three features of metabolic syndrome. In conclusions, clinical picture of type 2 diabetes in Thai youth varied from asymptomatic to severe illness (DKA). Almost all had clinical features of metabolic syndrome. Childhood obesity has become epidemic in our population. Such clinical picture should alert all pediatricians to be aware of chronic diseases and for making an early diagnosis and preventing long-term complications in the future.
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PMID:Clinical pictures of type 2 diabetes in Thai children and adolescents is highly related to features of metabolic syndrome. 1685 38

Diabetes mellitus (DM) type I was diagnosed in two children, a girl aged 10.9 years and a boy aged 10.3 years, who suffered from overweight. Both were treated with subcutaneous insulin injections and dietary adjustments. Some of the data in the literature suggest that overweight or obesity during childhood increases the risk of type-I DM. Important in this connection is the so-called 'accelerator hypothesis', which postulates a common basis for both type-I and type-2 DM with genetic predisposition, insulin resistance (caused by rapid weight gain) and autoimmunity, leading to beta-cell insufficiency, as 'accelerators'. It is important to consider a diagnosis of type-I DM in children with overweight or obesity, especially in case of abnormal weight loss associated with polydipsia and polyuria.
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PMID:[Childhood obesity as a risk factor for diabetes mellitus type I: the accelerator hypothesis]. 1731 92

Obesity and insulin resistance are highly correlated with metabolic disturbances. Both the excess and lack of adipose tissue can lead to severe insulin resistance and diabetes. Adipose tissue plays an active role in energy homeostasis, hormone secretion, and other proteins that affect insulin sensitivity, appetite, energy balance, and lipid metabolism. Rats with streptozotocin-induced diabetes during the neonatal period develop the classic diabetic picture of hyperglycemia, hypoinsulinemia, and insulin resistance in adulthood. Low body weight and reduced epididymal (EP) fat mass were also seen in this model. The aim of this study was to investigate the glucose homeostasis and metabolic repercussions on the adipose tissue following chronic treatment with antidiabetic drugs in these animals. In the 4th week post birth, diabetic animals started an 8-week treatment with pioglitazone, metformin, or insulin. Animals were then killed, EP fat pads were excised, and blood samples were collected for biological and biochemical assays. Pioglitazone and insulin treatments, but not metformin, reduced hyperglycemia, polydipsia, and polyphagia. Although all antidiabetic therapies improved insulin sensitivity, this was particularly noteworthy in the pioglitazone-treated rats. Furthermore, a recovery of adipose mass and insulin levels were observed in pioglitazone- and insulin-, but not metformin-treated animals. Treatments with insulin or pioglitazone were able to correct significantly, but not completely, the metabolic abnormalities, parallel to full recovery of adipose mass, indicating that not only the low insulin levels but also the lack of adipose tissue might play a significant role on the pathophysiology of this particular diabetes model.
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PMID:Metabolic recovery of adipose tissue is associated with improvement in insulin resistance in a model of experimental diabetes. 1845 Oct 64

The genetic model of diabetes mellitus was studied on mutant C57Bl/KsLepr(db/+) mice. These mice were characterized by high concentrations of glucose and glycosylated hemoglobin in the blood, polyuria, polyphagia, polydipsia, progressive obesity, biphasic morphological changes in insular islets of the pancreas (hyperplasia and atrophy), fatty degeneration of the liver, and hypoplasia of the spleen tissue and lymph nodes. Our results indicate that C57Bl/KsLepr(db/+) mice serve as an adequate model of type 2 diabetes mellitus. This model is suitable for testing of therapeutic methods for type 2 diabetes mellitus.
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PMID:Mutant C57Bl/Kslepr(db/+) mice as a genetic model of type 2 diabetes mellitus. 1885 8

A privately owned, obese, adult female raccoon (Procyon lotor) presented with polyuria, polydipsia, weight loss, and increased appetite. Diabetes mellitus was diagnosed based on laboratory findings, including hyperglycemia and glucosuria. As a result of the raccoon's age and obesity at the onset of clinical signs, the raccoon was thought to have type 2 diabetes mellitus, a diagnosis that was supported by paired glucose tolerance tests. Treatment consisted of dietary management and daily insulin therapy. The raccoon was gradually weaned off insulin with no return of clinical signs, further verifying the characterization of type 2 diabetes mellitus.
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PMID:Transient type 2 diabetes mellitus in a raccoon (Procyon lotor). 1911 Jul 6


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