scholarly journals Glucose transporter 2 concentrations in hyper- and hypothyroid rat livers

1999 ◽  
Vol 160 (2) ◽  
pp. 285-289 ◽  
Author(s):  
T Mokuno ◽  
K Uchimura ◽  
R Hayashi ◽  
N Hayakawa ◽  
M Makino ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Plasma Membranes ◽  
Glucose Transporter ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Abnormal Glucose Metabolism ◽  
Glucose Transporter 2 ◽  
Liver And Pancreas ◽  
Rat Livers

The deterioration of glucose metabolism frequently observed in hyperthyroidism may be due in part to increased gluconeogenesis in the liver and glucose efflux through hepatocyte plasma membranes. Glucose transporter 2 (GLUT 2), a facilitative glucose transporter localized to the liver and pancreas, may play a role in this distorted glucose metabolism. We examined changes in the levels of GLUT 2 in livers from rats with l-thyroxine-induced hyperthyroidism or methimazole-induced hypothyroidism by using Western blotting to detect GLUT 2. An oral glucose tolerance test revealed an oxyhyperglycemic curve (impaired glucose tolerance) in hyperthyroid rats (n=7) and a flattened curve in hypothyroid rats (n=7). GLUT 2 levels in hepatocyte plasma membranes were significantly increased in hyperthyroid rats and were not decreased in hypothyroid rats compared with euthyroid rats. The same results were obtained with a densitometric assay. These findings suggest that changes in the liver GLUT 2 concentration may contribute to abnormal glucose metabolism in thyroid disorders.

Chronic exercise increases insulin binding in muscles but not liver

1986 ◽  
Vol 251 (2) ◽  
pp. E196-E203
Author(s):  
A. Bonen ◽  
P. A. Clune ◽  
M. H. Tan
Keyword(s):  
Glucose Tolerance ◽  
Plasma Membranes ◽  
Serum Insulin ◽  
Exercise Bout ◽  
Insulin Binding ◽  
Tolerance Test ◽  
Time Of Day ◽  
Oral Glucose ◽  
Chronic Exercise ◽  
Binding Data

It has been postulated that the improved glucose tolerance provoked by chronic exercise is primarily attributable to increased insulin binding in skeletal muscle. Therefore, we investigated the effects of progressively increased training (6 wk) on insulin binding by five hindlimb skeletal muscles and in liver. In the trained animals serum insulin levels at rest were lower either in a fed (P less than 0.05) or fasted (P less than 0.05) state and after an oral glucose tolerance test (n = 8) (P less than 0.05). Twenty-four hours after the last exercise bout sections of the liver, soleus (S), plantaris (P), extensor digitorum longus (EDL), and red (RG) and white gastrocnemius (WG) muscles were pooled from four to six rats. From control animals, killed at the same time of day, muscles and liver were also obtained. Insulin binding to plasma membranes increased in S, P, and EDL (P less than 0.05) but not in WG (P = 0.07), RG (P greater than 0.1), or in liver (P greater than 0.1). There were insulin binding differences among muscles (P less than 0.05). Comparison of rank orders of insulin binding data with published glucose transport data for the same muscles revealed that these parameters do not correspond well. In conclusion, insulin binding to muscle is shown to be heterogeneous and training can increase insulin binding to selected muscles but not liver.

Status of Glucose Metabolism and the Factors Affecting It, in Children with Thalassemia Major.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3848-3848
Author(s):  
Anupam Sachdeva ◽  
Satya Prakash Yadav ◽  
Subash C. Arya ◽  
Virender K. Khanna ◽  
Archana D. Arya
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Age Of Onset ◽  
Thalassemia Major ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Normal Glucose

Abstract Abnormalities of the glucose metabolism are well documented in patients with Thalassemia Major who are frequently transfused and receiving therapy for chelation, due to excess iron deposition in the pancreas. The incidence of abnormalities in the glucose metabolism increase with age, with peak incidence between 16–20 years. The Indian (Asian) population is genetically predisposed to developing type 2 diabetes mellitus which is an additional risk factor for our Thalassemic population. Chelation is suboptimal in most of the patients due to economic reasons and ignorance. Impaired glucose tolerance (IGT) usually precedes the development of frank diabetes mellitus and intensive chelation in those with impaired glucose tolerance test may delay/prevent the onset of diabetes mellitus. Hence it is important to know the glyco-metabolic status of these children. At our Thalassemia endocrinology clinic, glucose tolerance test (GTT) is performed routinely in all subjects with Thalassemia major who have not already developed diabetes to identify the “at risk” population.GTT is performed by drawing a baseline fasting sample for blood glucose, oral glucose was given in a dose of 1.75mg/kg upto a maximum of 75 gms. Blood glucose level is measured 2 hours after oral glucose. According to the WHO criteria, Fasting plasma glucose between 110–126mg/dl is classified as impaired fasting and above 126mg/dl as diabetes. 2-hour plasma glucose value between 140–200mg/dl is classified as impaired glucose tolerance and above 200 mg/dl as diabetes. The purpose of this study was to analyze the status of the glucose metabolism of children and young adults with Thalassemia major who were attending our Thalassemia endocrinology clinic and to compare the factors affecting subjects with an abnormal glucose metabolism with those who have a normal glucose metabolism. The parameters compared were: effect of mean S. ferritin levels, age of onset of chelation and genetic predisposition. Retrospective analysis of our case records was done to determine the prevalence of diabetes and impaired glucose tolerance in children and young adults between 13 and 25 years of age. Of the 33 subjects evaluated, 16 out of 33 (48.5%) subjects had an abnormality of the glucose metabolism. 14/33 subjects (42.4%) had developed diabetes mellitus and 2 had an impaired GTT. Of the 16 affected subjects 9 were males and 7 were females (M:F = 1.28:1). The mean serum ferritin for this group was 5464ng/ml, 5503ng/ml for the diabetic group and 5425 for those with impaired GTT. (Range 2523–10904ng/ml). History of diabetes in a first or second degree relative was positive in 9 subjects(56.25%), negative in 2 and unknown in 5 subjects. Average age of onset of chelation was 8 years in this group. Oral glucose tolerance test was normal in 17/33(51.5%) subjects of which 10 were males and 7 were females (1.42:1). Average serum ferritin was 4747.4ng/ml in the group with a normal glucose tolerance. (1600–8294ng/ml). Family history of diabetes in a first or second degree relative was positive in 8 subjects(47%), negative in 4 and unknown in 5 subjects. Average age of onset of chelation was 6.5 years in the group with normal glucose metabolism. In conclusion of the 33 subjects evaluated, 48.5% had an abnormal glucose metabolism.

scholarly journals TNF signaling impacts glucagon-like peptide-1 expression and secretion

2018 ◽  
Vol 61 (4) ◽  
pp. 153-161 ◽  
Author(s):  
Sufang Chen ◽  
Wei Wei ◽  
Minjie Chen ◽  
Xiaobo Qin ◽  
Lianglin Qiu ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Deficient Mice

Numerous studies have implicated tumor necrosis factor α (TNFα) in the pathogenesis of type 2 diabetes. However, the role of its primary receptor, TNF receptor 1 (TNFR1), in homeostatic regulation of glucose metabolism is still controversial. In addition to TNFα, lymphotoxin α (LTα) binds to and activates TNFR1. Thus, TNFα and LTα together are known as TNF. To delineate the role of TNF signaling in glucose homeostasis, the present study ascertained how TNF signaling deficiency affects major regulatory components of glucose homeostasis. To this end, normal diet-fed male TNFR1-deficient mice (TNFR1−/−), TNFα/LTα/LTβ triple-deficient mice (TNF/LT∆3) and their littermate controls were subjected to intraperitoneal glucose tolerance test, insulin tolerance test and oral glucose tolerance test. The present results showed that TNFR1−/− and TNF/LT∆3 mice vs their controls had comparable body weight, tolerance to intraperitoneal glucose and sensitivity to insulin. However, their tolerance to oral glucose was significantly increased. Additionally, glucose-induced insulin secretion assessments revealed that TNFR1 or TNF/LT deficiency significantly increased oral but not intraperitoneal glucose-induced insulin secretion. Consistently, qPCR and immunohistochemistry analyses showed that TNFR1−/− and TNF/LT∆3 mice vs their controls had significantly increased ileal expression of glucagon-like peptide-1 (GLP-1), one of the primary incretins. Their oral glucose-induced secretion of GLP-1 was also significantly increased. These data collectively suggest that physiological TNF signaling regulates glucose metabolism primarily through effects on GLP-1 expression and secretion and subsequently insulin secretion.

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