Glucose tolerance and gastric emptying in thyrotoxic rats

Ikeda, Tadasu; Fujiyama, K.; Hoshino, Tazue; Takeuchi, Tatsuo; Tominaga, Masato; Mashiba, Hiroto

doi:10.1016/0026-0495(89)90234-5

Cited by 5 publications

(5 citation statements)

References 25 publications

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“…However, in a study of rats treated with T 4 for 10-30 days, the number of GLUT4 and the basal rate of 3OMG transport in the muscles of the hindquarter were increased, but the responsiveness of this rate to maximal levels of insulin was actually decreased [15]. It is likely that, in the latter study [15], plasma T 3 levels [31] were much higher than those in the present study or in the study of Weinstein et al [12], suggesting that, under extreme conditions of thyrotoxicity, most of the GLUT4 transporters may migrate to the plasma membrane: this could lead to a near-maximal response at low levels of insulin (i.e. a further increase in sensitivity) but to a decreased response when insulin is elevated.…”

Section: Glucose Transport and Phosphorylationmentioning

confidence: 90%

The effects of insulin on transport and metabolism of glucose in skeletal muscle from hyperthyroid and hypothyroid rats

Dimitriadis

Parry-Billings

Bevan

et al. 1997

Eur J Clin Investigation

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The effects of insulin on the rates of glucose disposal were studied in soleus muscles isolated from hyper- or hypothyroid rats. Treatment with triiodothyronine for 5 or 10 days decreased the sensitivity of glycogen synthesis but increased the sensitivity of lactate formation to insulin. The sensitivity of 3-O methylglucose to insulin was increased only after 10 days of treatment and was accompanied by an increase in the sensitivity of 2-deoxyglucose phosphorylation; however, 2-deoxyglucose and glucose 6-phosphate in response to insulin remained unaltered. In hypothyroidism, insulin-stimulated rates of 3-O-methylglucose transport and 2-deoxyglucose phosphorylation were decreased; however, at basal levels of insulin, 3-O-methylglucose transport was increased, while 2-deoxyglucose phosphorylation was normal. In these muscles, the sensitivity of lactate formation to insulin was decreased; this defect was improved after incubation of the muscles with prostaglandin E2. The results suggest: (a) in hyperthyroidism, insulin-stimulated rates of glucose utilization in muscle to form lactate are increased mainly because of a decrease in glycogen synthesis; when hyperthyroidism progresses in severity, increases in the sensitivity of glucose transport to insulin and in the activity of hexokinase may also be involved; (b) in hypothyroidism, the decrease in insulin-stimulated rates of glucose utilization is caused by decreased rates of glycolysis; (c) prostaglandins may be involved in the changes in sensitivity of glucose utilization to insulin observed in muscle in altered thyroid states.

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Section: Glucose Transport and Phosphorylationmentioning

confidence: 90%

The effects of insulin on transport and metabolism of glucose in skeletal muscle from hyperthyroid and hypothyroid rats

Dimitriadis

Parry-Billings

Bevan

et al. 1997

Eur J Clin Investigation

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“…Rapid gastric emptying and increased rates of intestinal absorption of glucose have been hypothesized to be responsible for impaired glucose tolerance in hyperthyroidism (4)(5)(6). However, in more recent studies, gastric emptying has been found to be decreased (7,8) or unchanged (9 -11).…”

Section: Gastric Emptying and Intestinal Absorptionmentioning

confidence: 92%

Insulin Action in Hyperthyroidism: A Focus on Muscle and Adipose Tissue

2010

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Hyperthyroidism leads to an enhanced demand for glucose, which is primarily provided by increased rates of hepatic glucose production due to increased gluconeogenesis (in the fasting state) and increased Cori cycle activity (in the late postprandial and fasting state). Adipose tissue lipolysis is increased in the fasting state, resulting in increased production of glycerol and nonesterified fatty acids. Under these conditions, increased glycerol generated by lipolysis and increased amino acids generated by proteolysis are used as substrates for gluconeogenesis. Increased nonesterified fatty acid levels are necessary to stimulate gluconeogenesis and provide substrate for oxidation in other tissues (such as muscle). In the postprandial period, insulin-stimulated glucose uptake by the skeletal muscle has been found to be normal or increased, mainly due to increased blood flow. Under hyperthyroid conditions, insulin-stimulated rates of glycogen synthesis in skeletal muscle are decreased, whereas there is a preferential increase in the rates of lactate formation vs. glucose oxidation leading to increased Cori cycle activity. In hyperthyroidism, the Cori cycle could be considered as a large substrate cycle; by maintaining a high flux through it, a dynamic buffer of glucose and lactate is provided, which can be used by other tissues as required. Moreover, lipolysis is rapidly suppressed to normal after the meal to facilitate the disposal of glucose by the insulin-resistant muscle. This ensures the preferential use of glucose when available and helps to preserve fat stores.

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“…Beta cell apoptosis via an unknown mechanism has been demonstrated in the pancreas in L-thyroxine administered rats (31). Additionally, it is thought that the phenomena rapid gastric emptying and glucose absorption in thyrotoxic patients result in postprandial hyperglycemia and an increased insulin response, thus causing insulin resistance (32,33). However, Fukuchi et al detected higher glucose levels and a lower insulin response to oral glucose loading in rats given intraperitoneal L-thyroxine and suggested that the abnormal glucose tolerance observed in cases of hyperthyroidism is related to a decreased pancreatic cell response rather than peripheral resistance (34).…”

Section: Discussionmentioning

confidence: 99%

Serum Adiponectin Levels and Changes in Glucose Metabolism before and after Treatment for Thyroid Dysfunction

2015

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Objective Adiponectin is an adipokine which is known to decrease in individuals associated with obesity and insulin resistance. In this study, we aimed to investigate the serum adiponectin levels and glucose metabolism in patients with thyroid dysfunction before and after treatment. Methods Newly diagnosed overt hypothyroid (n=20) and thyrotoxic (n=23) patients and healthy controls (n=20) with a body mass index of <30 kg/m 2 were evaluated prospectively. Patients with a known state of insulin resistance, including prediabetes and overt diabetes, and individuals with chronic diseases were excluded. Thyroid function and fasting plasma glucose (FPG), insulin, homeostatic model assessment (HOMA) insulin resistance (HOMA-IR) and HOMA-beta cell function (HOMA-beta), lipid and adiponectin levels were investigated in the basal state and after the restoration of euthyroidism. Results The basal fasting FPG levels were lower in the hypothyroid patients than the control subjects (p= 0.02) and similar between the thyrotoxic patients and control subjects (p=0.127). The basal HOMA-beta levels were higher in the patients with hypothyroidism than in those with thyrotoxicosis (p=0.015). Following the restoration of euthyroidism, the FPG levels significantly increased in the hypothyroid patients (p=0.002) and decreased in the thyrotoxic (p=0.001) patients. The basal plasma adiponectin levels were 14.55±8.4 mcg/ mL, 13.79±9.13 mcg/mL and 11.68±6.0 mcg/mL in the hypothyroid and thyrotoxic patients and healthy controls, respectively (p=0.503). The adiponectin levels decreased significantly in the patients with hypothyroidism (p=0.047), whereas they did not change in the patients with thyrotoxicosis (p=0.770) after achieving euthyroidism. Conclusion In this study, following the restoration of euthyroidism, the FPG levels increased in the hypothyroidism patients and decreased in the thyrotoxicosis patients, despite the lack of changes in the HOMA-IR and HOMA-beta levels. Meanwhile, the hypothyroid, thyrotoxic and euthyroid subjects had similar basal adiponectin levels, and a significant decrease in the adiponectin levels was observed after treatment for hypothyroidism, despite the absence of changes after treatment for thyrotoxicosis, indicating the need for further studies with a larger sample size.

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Glucose tolerance and gastric emptying in thyrotoxic rats

Cited by 5 publications

References 25 publications

The effects of insulin on transport and metabolism of glucose in skeletal muscle from hyperthyroid and hypothyroid rats

The effects of insulin on transport and metabolism of glucose in skeletal muscle from hyperthyroid and hypothyroid rats

Insulin Action in Hyperthyroidism: A Focus on Muscle and Adipose Tissue

Serum Adiponectin Levels and Changes in Glucose Metabolism before and after Treatment for Thyroid Dysfunction

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