Hepatic estrogen and androgen receptors and binding proteins in streptozotocin-diabetic male Wistar rats

Abstract

We have previously shown that there are decreases in the sex differences seen in certain hepatic drug and steroid metabolising enzymes in rats with early (4 day) streptozotocin-induced diabetes. We postulated that hepatic sex hormone receptors or binding proteins might be involved in modulation of the sex differences noted in metabolism. In the present study, we measured the binding kinetics of the hepatic cytosolic estrogen receptor and androgen receptor, along with the high capacity-low affinity estrogen binding protein. At 4 or 10 days post-streptozotocin (60 mg/kg intravenously), there was no change in the maximum binding capacity of the estrogen receptor, nor in the hormone affinity of any of the three proteins. However, the binding capacity of the androgen receptor and estrogen binding protein in the diabetic animals was decreased to less than half of control levels. This effect could not be reversed by hormone replacement with any of the following regimens: protamine zinc insulin, 10 U/kg subcutaneously once a day; Toronto insulin, 15 U/kg subcutaneously twice a day; testosterone enanthate, 1 mg/kg s.c. once a day; triiodothyronine, 30 micrograms/kg s.c. daily; ovine growth hormone: 0.02 U/h s.c., 30 micrograms s.c. 7 times daily, 30 micrograms i.v. 4 times daily; or various combinations of these hormones. Stress, such as 4 intravenous injections of saline per day, was noted to decrease the binding capacity of the estrogen binding protein. Therefore, we measured the basal serum corticosterone levels, which were not significantly different from control values in untreated or insulin-treated diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of sex hormones on vascular responses in the aorta of streptozotocin-diabetic male rats

“…Our work does not provide a conclusive explanation for this clinically relevant discrepancy and calls for future studies on this topic. However, evidence indicates that experimental diabetes strongly affects the expression pattern of sex steroid receptors in non-vascular tissues (Smith et al 1987;Nadal et al 1998). Should this be the case in arterial tissues as well, circulating steroid hormones would be likely to impact on vascular function in a sharply different fashion in diabetic, as opposed to non-diabetic animals.…”

The Role of Vasopressin in Hypothalamo‐Pituitary‐Adrenal Axis Activation during Stress: An Assessment of the Evidence

“…We used different chronic stress paradigms for 14 days and measured the typical somatic parameters (body, adrenal gland, and thymus weight changes) in Brattleboro rats to see whether AVP is needed for the appearance of chronic stress syndrome. Daily 60‐min restraint stress was used as a combined psychological‐physical stress stimulus,29,30 morphine injection for 16 days (10, 20, 40, 80, and 160 mg/kg increasing dose, twice daily)32 was used as a drug abuse model, and hypertonic saline injection31 was supposed to increase parvocellular AVP and streptozotocin‐induced diabetes mellitus (STZ) made for metabolic stress (STZ: 60 mg/kg/2mL saline iv into the tail) 33. Each stressor decreased the body weight gain and the thymus weight and induced significant adrenal gland hypertrophy.…”

“…All types of chronic stress induced significant body and thymus weight decrease and adrenal hypertrophy, whereas the effect of genotype was not significant in any type of stress on any studied parameter, and there was no interaction between genotype and stress. di/+, heterozygous, control rats; di/di, homozygous diabetes insipidus, AVP‐deficient rats; C, control, without chronic stress or with vehicle injection; R, daily 1‐hr restraint29,30 ( n = 32 to 39); Mo, morphine injections twice daily in increasing dose32 ( n = 21 to 41); Hs, hypertonic saline injection 1.5 M NaCl, 1.5 mL/100 g bw31 ( n = 5 to 8); STZ, iv 60 mg/kg streptozotocin in citrate buffer33 ( n = 17 to 25).…”