THYROID IODINE METABOLISM IN STREPTOZOTOCIN-DIABETIC RATS

1978 ◽  
Vol 88 (3) ◽  
pp. 506-516 ◽  
Author(s):  
Trinidad Jolín ◽  
Concepción González ◽  
Margarita González

ABSTRACT Experiments have been performed to assess the effect of diabetes on thyroid function in male Wistar rats. Diabetes was induced by a single streptozotocin injection. As compared to normals, the diabetic rats displayed: 1) decreased rate of stable iodine uptake by the gland, as measured with a double isotopic technique; 2) decreased in vitro iodide uptake by the thyroid; 3) decreased T/S [I-] ratio after acute treatment with propylthiouracil; and 4) alteration in the distribution of labelled iodoamino acids in the gland. Furthermore, diabetic rats maintained lower plasma TSH levels than normals, in spite of the fact that plasma PBI concentration was slightly but consistently lower in diabetic than in normals, and that the pituitary TSH content was not affected by the lack of normal insulin levels. Injections of TSH (5 U/100 g body weight/day) for 5 days, into diabetic rats caused a return of thyroid function toward normal. Insulin administration resulted in an increase of thyroid weight, an increase of thyroid function, and an increase of pituitary TSH secretion in diabetic rats after the daily injection of 1, 2 or 3 U/100 g body weight/day for 7 days. The decreased pituitary TSH secretion in diabetic rats might involve a disturbance in the feed-back relationship between the thyroid and the pituitary, although other mechanisms could be involved.

1977 ◽  
Vol 86 (1) ◽  
pp. 128-139 ◽  
Author(s):  
Isabel Pericás ◽  
Trinidad Jolín

ABSTRACT Studies of pituitary and thyroid function have been carried out in normal (intact) and diabetic Wistar rats. Diabetes was induced by a single streptozotocin injection (7 mg/100 g body weight). The animals were fed a low iodine diet (LID), and received a daily sc injection of either KClO4 (20 mg/100 g body weight) or propylthiouracil (PTU) (1.5 mg/100 g body weight) to induce hypothyroidism. Control groups received the same LID but supplemented with 0.8 μg I/g dry weight. In intact rats goitrogen-treatment induces an increase in thyroid weight and in plasma TSH concentration. However, the plasma TSH response to goitrogen-treatment in diabetics indicates that pituitary TSH secretion increases following a reduction in plasma PBI, but the response is less marked than in controls. The difference in plasma TSH between control and diabetic rats provides an explanation for the findings that diabetes diminishes the thyroid growth response to goitrogen-treatment. Moreover, in intact rats the low pituitary TSH content is a consequence of the increase in pituitary TSH secretion, while in the diabetics the low pituitary TSH content cannot be explained by an increase in TSH secretion. The effect of diabetes on the pituitary-thyroid axis cannot be attributed specifically to poor growth, because the changes in pituitary-thyroid function which are observed in the diabetic groups are not seen in intact rats with a growth rate similar to that of insulin deficient rats. Insulin administration to goitrogen-treated diabetic rats results in 1) an increase in the ability of the thyroid tissue to respond to its trophic hormone, 2) an increase in pituitary TSH secretion in response to the lowering of plasma PBI and, 3) an increase in thyroid growth response to goitrogen-treatment. Results are discussed in relation to the assumption that the lack of adequate insulin levels, or its metabolic defects, diminishes the full response of the thyroid to TSH, and affects the pituitary TSH secretion probably as a consequence of altered hypothalamic control of the pituitary function.


1978 ◽  
Vol 88 (4) ◽  
pp. 721-728 ◽  
Author(s):  
Eladio Montoya ◽  
Concepción González ◽  
Luis Lamas ◽  
Trinidad Jolín ◽  
Margarita González

ABSTRACT Studies on the hypothalamus-pituitary-thyroid axis have been carried out in control and in diabetic male Wistar rats during adaptation to a 125I-labelled low iodine diet. Diabetes was induced by a single streptozotocin injection (7 mg/100 g body weight). Thyroid weight, thyroid 127I and 125I content, [125I]iodoamino acid distribution in thyroid digests, plasma PBI, plasma and pituitary TSH and hypothalamic TRH by radioimmunoassay were measured between 5 and 30 days after saline or streptozotocin injection, corresponding to 15 and 40 days after onset of the 125I-LID. As compared to controls, diabetic animals have smaller thyroids. The 125I and 127I in diabetic thyroids between 5 and 10 days was lower than in control glands; at longer intervals both 125I and 127I increased with time in diabetics, while no remarkable changes were seen in the control glands. Furthermore, the percentage of T3 and the MIT/DIT and T3/T4 ratios in thyroids of diabetic were lower than in the corresponding control group at all intervals. These results are compatible with a deficiency of TSH stimulation and/or with a high thyroidal iodine content. Compared to the controls, each group of diabetic rats presented a significantly lower plasma TSH concentration, in spite of the fact that its plasma PBI is more or similarly reduced in diabetic than in controls. Furthermore, the decreased pituitary TSH secretion in diabetic rats at early intervals is lower than in controls although the pituitary TSH and hypothalamic TRH remain within normal ranges. It is concluded that the decrease in pituitary TSH secretion may be the result of a reduction of pituitary TRH stimulation, secondary to a diminished secretion and/or synthesis of TRH by the hypothalamus.


2020 ◽  
Vol 10 (4-s) ◽  
pp. 138-141
Author(s):  
Dalila Bencheikh ◽  
Seddik Khennouf ◽  
Saliha Dahamna

The seeds of Trigonella foenum-graecum (fenugreek) are used for treatment of diabetes mellitus in traditional medicine. This paper examines the protection effects of fenugreek from the damage induced by streptozotocin diabetes rats. Tannins content of T. foenum-graecum was also estimated in vitro. Normoglycemic male Wistar rats, weighing 170-250 g, were selected and randomly divided into five groups (n= 6): normal control, diabetic + TFGE (200mg/kg), diabetic+ TFGE (600mg/kg), diabetic + Glibil (3mg/kg), untreated group. Diabetes was induced after a single intraperitoneal injection of streptozotocin (50 mg/kg body weight) and Fenugreek was given every day via orogastric tube for 18 days. At the end of experiment, rats were sacarificed. Organ weight was estimated of all groups. Trigonella foenum-graecum administration significantly improved the polydipsia, polyphagia, and it also compensated weight loss of diabetic rats (P<0.05, P < 0.01). Moreover, fenugreek had a significant concentration of tannins (806.22 ±0.036 µg TAE/gE). The results revealed that fenugreek improves the damage in diabetic rats that in some ways validates the traditional use of this plant in treatment of diabetes. Keywords: Antidiabetic activity, Protective effect, Streptozotocin, Tannins, Trigonella foenum-graecum


2017 ◽  
Vol 54 (3) ◽  
pp. 336
Author(s):  
Kavitha K. ◽  
Ponne S.

The present study was designed to assess the in vitro and in vivo anti-diabetic efficacy of <em>O. sanctum</em> seed and its phytochemical screening. In vitro inhibitory effect on carbohydrate digestive enzymes like α-amylase and α-glucosidase and in vivo parameters such as fasting blood glucose and body weight changes were studied, a potent inhibitory effect was observed on activities of digestive enzymes and a marked decrease in the glucose level in the <em>O. sanctum</em> seed extract treated streptozotocin induced diabetic rats was noted. Further a marked reduction in body weight was also observed.


1977 ◽  
Vol 86 (2) ◽  
pp. 336-343 ◽  
Author(s):  
A. A. Zaninovich ◽  
T. J. Brown ◽  
R. Boado ◽  
N. R. Bromage ◽  
A. J. Matty

ABSTRACT The metabolism of thyroxine (T4) was determined in untreated and in insulin-treated diabetic rats. The results were compared with those obtained in a control group. Male Wistar rats weighing approximately 200 g were made diabetic by the intraperitoneal administration of streptozotocin (6.5 mg/100 g body weight) and 17 of those with blood sugar levels above 500 mg/100 ml were studied. In addition, 11 insulin-treated diabetic and 18 control rats were investigated. All the animals were injected intravenously with a tracer dose of [125I]T4 (1 μCi and 0.015 μg). After this blood samples were obtained by cardiac puncture at 16, 24, 40 and 48 h. The 24-h urinary excretion of inorganic 125iodide was also determined. The parameters of T4 metabolism were obtained by the least squares method and by an extrapolation technique. In untreated diabetic rats the fractional T4 turnover was 4.4%h, the distribution space 36.7 ml/100 g body weight, metabolic clearance 1.57 ml/100 g/h and urinary clearance 0.33 ml/100 g/h. The 24-h urinary excretion of 125iodide was 21.3 % of the injected radioactivity. Of these values the distribution space (P < 0.001) and metabolic clearance (P < 0.05) were significantly increased above those in the control animals. In insulin-treated rats all parameters were within normal values. Among these groups the serum T4 concentration was measured in 6 control, 5 untreated diabetic and 6 insulin-treated animals. The untreated diabetic animals had a significantly decreased serum T4 level but this was balanced by an enlarged distribution space so that the final hormone degradation was normal. In addition, the T4 binding activity of serum was assessed by the in vitro red cells uptake of [125I] T4 and by determining the proportion of serum free T4. Both these indices indicated a decrease in serum binding activity in the diabetic animals. The data suggest that the fall in serum T4 levels observed in the untreated diabetic rats was the result of decreased plasma binding of T4 and an increase in distribution space precipitated by lack of insulin.


1981 ◽  
Vol 240 (3) ◽  
pp. G225-G231
Author(s):  
R. P. Cornell

In contrast to previous studies of neutrophils from diabetic animals and humans in vitro and of macrophages from diabetic humans in vivo, which reported phagocytic depression, reticuloendothelial system (RES) hyperphagocytosis of colloidal carbon was observed in rats at 14 and 28 days after diabetes induction with streptozotocin (STZ). Carbon clearance half times were significantly enhanced to 6.3 +/- 0.79 and 8.1 +/- 1.04 min at 14 and 28 days post-STZ, respectively, compared with the nondiabetic value (12.7 +/- 0.98 min). The severity of uncontrolled STZ-induced diabetes in rats was confirmed by significant hypoinsulinemia, hyperglucagonemia, hyperglycemia, and hyperlipidemia. Although body weights of STZ-diabetic animals declined progressively, liver weights as a percent of body weight increased above the control value at 14 and 28 days post-STZ. In fact, expression of carbon phagocytosis as the corrected phagocytic index, which accounts for changes in liver and spleen weights relative to body weight, eliminated the significant difference between STZ-diabetic and nondiabetic animals. Antibiotic treatment of diabetic rats failed to alter the hyperphagocytosis, implying that a chronic bacterial infection was not the cause of phagocytic stimulation. Daily insulin replacements, but not a single large insulin dose to 14-day post-STZ rats, reversed the enhanced phagocytosis of colloidal carbon.


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