Calcium Signaling in the Ventricular Myocardium of the Goto-Kakizaki Type 2 Diabetic Rat.

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diabetes mellitus 3 endocrinologydiseases
hyperglycemia 13 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases
obesity 6 endocrinologydiseases
type 2 diabetes mellitus 2 endocrinologydiseases

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diabetes mellitus 728 UKPublication date (collection): /2018Publication date (epub): 4/2018AbstractThe association between diabetes mellitus (DM) and high mortality linked to cardiovascular disease (CVD) is a major concern worldwide. Clinical
diabetes mellitus 963 studies have demonstrated a variety of diastolic and systolic dysfunctions in patients with type 2 diabetes mellitus (T2DM) with the severity of abnormalities depending on the patients' age and duration of diabetes. The
diabetes mellitus 2092 cardiomyopathy in both type 1 and type 2 diabetes. One of the most widely used animal models of type 2 diabetes mellitus (T2DM) is the Goto-Kakizaki (GK) rat. The GK rat is a polygenic nonobese model of T2DM. This model is
hyperglycemia 2539 pathogenesis of diabetes in the GK rat [[2]]. The general characteristics of the GK rat include fasting hyperglycemia , impaired insulin secretion in response to glucose both in vivo and in isolated pancreata, raised glycosylated
hyperglycemia 3280 prediabetic period (first three weeks after birth), animals have reduced body weight and do not show hyperglycemia . After weaning, many changes occur which include hyperglycemia, impaired glucose-induced insulin secretion
hyperglycemia 3343 reduced body weight and do not show hyperglycemia. After weaning, many changes occur which include hyperglycemia , impaired glucose-induced insulin secretion (due to defective prenatal β-cell proliferation and reduction
hyperglycemia 3602 sensitivity in the liver, and moderate insulin resistance in peripheral tissues [[12], [13]].Persistent hyperglycemia over time provokes pancreatic islet inflammation, oxidative stress, fibrosis, and finally β-cell dysfunction.
hyperglycemia 5151 example, in adult GK rats, significant morphological alterations in kidneys occur in response to chronic hyperglycemia which are similar to that in human diabetic patients [[18], [19]]. These morphological changes in kidneys
hyperglycemia 5563 characterized by insulin resistance and the inability of the β-cell to sufficiently compensate, which leads to hyperglycemia [[21]]. In addition, T2DM is closely associated with obesity which is one of the main pathological causes
hyperglycemia 6261 secretion required to compensate for the insulin resistance as part of the obesity (obesity-induced hyperglycemia ) [[13], [23]].Lepob/ob mice, Leprdb/db mice, and Zucker diabetic fatty rats are the most commonly used
hyperglycemia 7285 secretion. Furthermore, the development of insulin resistance does not seem to be the main initiator of hyperglycemia . Instead, the defective glucose metabolism is regarded to be due to reduced β-cell mass [[25]] and/or
hyperglycemia 7684 rises significantly after a glucose challenge [[13], [27]]. The GK model is characterized by early hyperglycemia , hyperinsulinemia, and insulin resistance, [[1], [12]]. Other examples of non-obese animal models of
hyperglycemia 9253 chemistry may be attributed to the age of the animals and dietary regime. In summary, the GK rat displays hyperglycemia , insulin resistance, and disturbances in lipid profile.4. Body and Heart Weight in the Goto-Kakizaki
hyperglycemia 10796 model provide evidence for regional cardiac hypertrophy.Earlier studies have reported that chronic mild hyperglycemia produces molecular and structural correlates of hypertrophic myopathy in GK rats [[40]]. Several mechanisms
hyperglycemia 10926 molecular and structural correlates of hypertrophic myopathy in GK rats [[40]]. Several mechanisms whereby hyperglycemia may induce left ventricle remodeling have been proposed. One of these mechanisms is the increased activity
hyperglycemia 23756 models of both type 1 and type 2 diabetes. For example, in streptozotocin- (STZ-) induced diabetic rats, hyperglycemia was associated with lower rates of mitochondrial Ca2+ uptake [[107]]. This reduction can be explained
hyperinsulinemia 7699 significantly after a glucose challenge [[13], [27]]. The GK model is characterized by early hyperglycemia, hyperinsulinemia , and insulin resistance, [[1], [12]]. Other examples of non-obese animal models of T2DM are the C57BL/6
obesity 5630 sufficiently compensate, which leads to hyperglycemia [[21]]. In addition, T2DM is closely associated with obesity which is one of the main pathological causes of insulin resistance [[15], [22]]. Many animal models
obesity 5859 as a result of naturally occurring mutations or genetic manipulation and are useful in understanding obesity -induced insulin resistance and its effects. These are divided into monogenic models, polygenic models,
obesity 6236 lack sufficient insulin secretion required to compensate for the insulin resistance as part of the obesity (obesity-induced hyperglycemia) [[13], [23]].Lepob/ob mice, Leprdb/db mice, and Zucker diabetic fatty
obesity 6245 sufficient insulin secretion required to compensate for the insulin resistance as part of the obesity ( obesity -induced hyperglycemia) [[13], [23]].Lepob/ob mice, Leprdb/db mice, and Zucker diabetic fatty rats are
obesity 6398 mice, Leprdb/db mice, and Zucker diabetic fatty rats are the most commonly used models of monogenic obesity . They have a disrupted leptin signaling pathway, leading to hyperphagia and obesity [[13]]. Polygenetic
obesity 6482 models of monogenic obesity. They have a disrupted leptin signaling pathway, leading to hyperphagia and obesity [[13]]. Polygenetic animal models, however, provide more accurate models of the human condition [[15]].
type 2 diabetes mellitus 956 preclinical studies have demonstrated a variety of diastolic and systolic dysfunctions in patients with type 2 diabetes mellitus (T2DM) with the severity of abnormalities depending on the patients' age and duration of diabetes. The
type 2 diabetes mellitus 2085 diabetic cardiomyopathy in both type 1 and type 2 diabetes. One of the most widely used animal models of type 2 diabetes mellitus (T2DM) is the Goto-Kakizaki (GK) rat. The GK rat is a polygenic nonobese model of T2DM. This model is

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