[Effects of sequoyitol on expression of NADPH oxidase subunits p22 phox and p47 phox in rats with type 2 diabetic liver disease].
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Abstract:
This study is to observe the effects of sequoyitol on the expression of NADPH oxidase subunits p22 phox and p47 phox in rats with type 2 diabetic liver diseases. The model of high fat and high sugar diet as well as intraperitoneal injection of small dose of streptozotocin (STZ, 35 mg x kg(-1)) induced diabetic rat liver disease was used. After sequoyitol (50, 25 and 12.5 mg x kg(-1)) was administrated for 6 weeks, the contents of blood glucose (BG), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total antioxidant capacity (T-AOC), hydrogen peroxide (H2O2), NO and insulin (Ins) were measured, liver p22 phox and p47 phox mRNA content was determined with real-time PCR and the expression of p22 phox and p47 phox protein was examined by Western blotting. In addition, pathological changes in liver were observed with HE staining. Sequoyitol could reduce the content of fasting blood glucose, ALT, AST, Ins and H2O2, restore insulin sensitive index (ISI) and weight, elevate liver tissue T-AOC and NO content, reduce the NADPH oxidase subunit liver tissue p22 phox and p47 phox mRNA and protein expression, as well as ameliorate liver pathologic lesions. The results showed that sequoyitol can ease the type 2 diabetic rat liver oxidative stress by lowering NADPH oxidase expression.Keywords:
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Effects of Serotonin on Blood Glucose and Insulin Levels of Glucose- and Streptozotocin-Treated Mice
Effects of serotonin (5-HT) on plasma glucose and serum insulin levels were studied in mice. In normal mice, 5-HT induced a dose-dependent hypoglycemia and an increase in serum insulin levels. 5-HT significantly inhibited glucose-induced hyperglycemia and increased glucose-stimulated insulin release. However, in streptozotocin-induced diabetic mice, 5-HT changed neither the glucose nor insulin levels. These results strongly suggest that 5-HT-induced hypoglycemia is brought on by increasing serum insulin levels.
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The present study was performed to further clarify the possible role played by insulin deficiency on the steroidogenic capacity of the rat testis. Sprague-Dawley rats weighing 250-300 g were used in all experiments. Diabetes was induced by i.p. injection (40 mg/kg b.w.) of streptozotocin and was monitored at 2-day intervals by measuring body weight and serum glucose, glucosuria and ketonuria levels. The effect of insulin therapy on pituitary LH content and plasma LH concentrations, as well as on the cyclic AMP level in interstitial cell incubation medium and plasma testosterone concentrations, was measured 30 days after the induction of diabetes by radioimmunoassay. Streptozotocin-induced diabetes resulted in significantly reduced pituitary LH (16%, P less than 0.025) and plasma LH (34%, P less than 0.02); insulin treatment completely restored these levels. Similarly, the cyclic AMP content of interstitial cell incubation medium and the plasma testosterone concentrations were dramatically decreased in the diabetic state (50%, P less than 0.005 and 63%, P less than 0.025, respectively) and combined treatment with insulin plus hCG appeared slightly more effective than treatment with either of these hormones alone, suggesting a possible synergistic action. It is concluded that decreased testicular steroidogenesis in the diabetic rat may represent, at least in part, a direct consequence of insulin deficiency at the hypothalamic and/or pituitary levels. However, our findings would also be consistent with other reports suggesting that insulin may play a direct role in the rat testis.
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Insulin binding to rat adrenal glands was studied in vivo by i.v. injection of 125I-insulin either alone or together with an excess of unlabelled hormones (insulin, glucagon, prolactin, or growth hormone). In addition, isolated glands from normal or streptozotocin diabetic rats (STZ) were incubated in vitro with 125I-insulin and varying concentrations of unlabelled insulin. Both experiments showed specific binding sites in the adrenal glands. Furthermore the glands from diabetic rats bound more insulin than the glands from controls.
Basal (medicine)
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Diabetic ketoacidosis
Ketoacidosis
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The decrease of insulin binding to plasma membranes of liver, adipose, and muscle tissues observed in obese-hyperglycemic (ob/ob) mice was reversed towards normal by prolonged fasting or streptozotocin treatment. The extent of this reversal was related to that of the decrease in hyperinsulinemia of the obese mice. In contrast, binding of glucagon to liver plasma membranes was little influenced by fasting or streptozotocin treatment of obese animals. The relationship between insulin binding and metabolic effects of the hormone did not appear to be identical in all tissues. In muscle, insulin binding and insulin effect on glucose uptake and metabolism changed in parallel--i.e., when binding increased, tissue sensitivity to the hormone increased. In the liver, the increase in insulin binding that followed fasting or streptozotocin treatment was not accompanied by any detectable metabolic effect of insulin on hepatic metabolism. A similar situation appeared to prevail in adipose tissue. The varying relationships observed between the state of insulin binding to membranes and the target tissue responsiveness to the hormone probably reflect the multiplicity of the factors operative in these processes and help us to understand why the over-all obese-hyperglycemic syndrome of ob/ob mice cannot be improved simply by decreasing endogenous hyperinsulinemia.
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Insulin deficiency as seen in insulin-dependent diabetes mellitus causes an activation of lipolysis in adipose tissue that results in hydrolysis of stored triglycerides and release of large amounts of fatty acids into the plasma, leading to diabetic ketoacidosis (DKA). Hormone-sensitive lipase (HSL) is thought to be the rate-limiting enzyme of lipolysis in adipose tissue. This study was designed to examine the effects of insulin deficiency on the regulation of HSL in isolated adipocytes. Insulin deficiency was induced by a single dose of streptozotocin. After 8 days, some animals were treated with insulin, and all animals were killed 10 days after induction of insulin deficiency. Compared with levels in control rats, 10 days of insulin deficiency increased HSL activity twofold (P < .05), as assayed for neutral cholesterol esterase activity, and insulin treatment returned HSL activity to normal. HSL protein was increased twofold (P < .05) in streptozotocin-induced diabetic rats, as estimated by immunoblotting, but remained elevated after insulin treatment. Levels of HSL mRNA assessed by Northern blot analysis also increased twofold (P < .01) in adipose cells isolated from streptozotocin-induced diabetic rats, and remained elevated after insulin treatment. In conclusion, our studies suggest that 10 days of insulin deficiency increases HSL expression via pretranslational mechanisms and short-term insulin treatment returns HSL activity to normal via posttranslational mechanisms in adipose tissue.
Hormone-sensitive lipase
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According to the “glucose toxicity” hypothesis, hyperglycemia contributes to defective β-cell function in type 2, non-insulin-dependent diabetes mellitus. This concept is supported by substantial data in rodent models of diabetes. However, the ability of glucose to stimulate the accumulation of insulin mRNA, a critical feature of normal β-cell physiology, has not been investigated in in vivo models with chronic hyperglycemia. The aim of this study was to determine whether glucose-induced insulin mRNA accumulation is impaired in the neonatal streptozotocin-treated rat (n0-STZ rat), a model of non-obese, non-insulin-dependent diabetes mellitus. Islets of Langerhans isolated from n0-STZ and control rats were cultured for 24 h in the presence of 2.8 or 16.7 mmol/l glucose, and insulin mRNA levels were measured by Northern analysis. Insulin mRNA levels were increased more than twofold by glucose in control islets. In contrast, no significant effect of glucose was found on insulin mRNA levels in n0-STZ islets. We conclude that insulin gene regulation by glucose is impaired in n0-STZ rat islets.
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Evidence for regulation of circulating leptin by insulin is conflicting. Diabetes was induced in rats with streptozotocin (STZ; 40 mg ⋅ kg −1 ⋅ day −1 × 2 days) to examine the effect of insulin-deficient diabetes and insulin treatment on circulating leptin. After 12 wk, plasma leptin concentrations in untreated rats were all <0.4 ng/ml versus 4.9 ± 0.9 ng/ml in control animals ( P < 0.005). In rats treated with subcutaneous insulin implants for 12 wk, which reduced hyperglycemia by ∼50%, plasma leptin was 2.1 ± 0.6 ng/ml, whereas leptin concentrations were 6.0 ± 1.6 ng/ml in insulin-implanted rats receiving supplemental injections of insulin for 4 days to normalize plasma glucose ( P< 0.005 vs. STZ untreated). In a second experiment, plasma leptin was monitored at biweekly intervals during 12 wk of diabetes. In rats treated with insulin implants, plasma leptin concentrations were inversely proportional to glycemia ( r= −0.64; P < 0.0001) and unrelated to body weight ( P = 0.40). In a third experiment, plasma leptin concentrations were examined very early after the induction of diabetes. Within 24 h after STZ injection, plasma insulin decreased from 480 ± 30 to 130 ± 10 pM ( P < 0.0001), plasma glucose increased from 7.0 ± 0.2 to 24.8 ± 0.5 mM, and plasma leptin decreased from 3.2 ± 0.2 to 1.2 ± 0.1 ng/ml (Δ = −63 ± 3%, P < 0.0001). In a subset of diabetic rats treated with insulin for 2 days, glucose decreased to 11.7 ± 3.9 mM and leptin increased from 0.5 ± 0.1 to 2.9 ± 0.6 ng/ml ( P< 0.01) without an effect on epididymal fat weight. The change of leptin was correlated with the degree of glucose lowering ( r = 0.75, P < 0.05). Thus insulin-deficient diabetes produces rapid and sustained decreases of leptin that are not solely dependent on weight loss, whereas insulin treatment reverses the hypoleptinemia. We hypothesize that decreased glucose transport into adipose tissue may contribute to decreased leptin production in insulin-deficient diabetes.
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Elevated concentrations of TRH have been detected in the rat pancreas during the early days of life. The purpose of this study was to investigate further the cellular location of this peptide in the pancreas using streptozotocin (STZ) injected at birth. Pancreatic TRH and insulin contents were measured at different ages from birth until 35 days in rats injected with STZ and results compared with controls injected with the vehicle. A transitory hyperglycemic state was observed from day 1 to day 5 (maximum value 2.9 ± 0.31 g/liter). After this period, although slightly hyperglycemic, STZ rats were not glucosuric. TRH and insulin contents followed two distinct patterns from days 1 to 5 and days 5 to 35. During the first period, an acute depletion of both substances was observed, the lower value observed reaching 2.7% and 9% of control values, respectively, for TRH and insulin. The TRH surge at day 2 was blunted. During the second period, insulin content increased to reach 42% of controls. On the contrary, recovery of TRH was not observed; TRH content was 9% of control at day 35. These results indicate that TRH is located in STZ-sensitive cells, in agreement with recent immunohistochemical data. The impaired capacity for TRH recovery remained unexplained and seems to indicate a difference in the biogenesis of insulin and TRH. (Endocrinology114: 2369, 1984)
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