Capsaicin-Sensitive Sensory Nerves in Recovery of Gastric Mucosal Integrity after Damage by Sodium Taurocholate in Rats
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Abstract:
We compared the recovery process of gastric mucosal integrity after damage by 20 mM sodium taurocholate (TC) in control, sensory deafferented and indomethacin-treated rats. Under anesthetized conditions, the stomach was mounted on a chamber and perfused with saline or 50 mM HCl. Application of TC (30 min) to the saline-perfused stomach produced a marked reduction in the potential difference (PD) (surface epithelial damage), followed by increases of gastric mucosal blood flow (GMBF) and luminal pH (alkalinization), but there was a rapid recovery of PD without development of gross lesions. Chemical ablation of capsaicin-sensitive sensory nerves had no influence on the PD reduction and luminal alkalinization, but significantly inhibited the rise in GMBF and the PD recovery. Indomethacin pretreatment (5 mg/kg, s.c.) significantly inhibited these changes seen after exposure to TC, except for PD reduction. In contrast, TC caused a sizable amount of H+ back-diffusion and a more pronounced and persistent rise in GMBF in the stomach perfused with 50 mM HCl, yet only minimal damage was observed in the control animals. Under these conditions, both sensory deafferentation and indomethacin inhibited such GMBF responses, leading to hemorrhagic damage without affecting the degree of H+ back-diffusion. These results suggest that capsaicin-sensitive sensory nerves contribute to the recovery of gastric mucosal integrity after damage, probably by maintaining GMBF responses associated with H+ back-diffusion and preventing the later extension to gross damage in the presence of acid.Keywords:
Capsaicin
Taurocholic acid
Sensory nerve
The effects of neonatal capsaicin upon selected metabolic and hormonal variables were investigated in hereditarily diabetic Goto-Kakizaki rats. Capsaicin failed to affect significantly the intake of food and fluid, the gain in body weight, the plasma glucose and insulin concentrations, and the insulin content of isolated pancreatic islets. However, the neonatal injection of capsaicin suppressed the stress-induced decrease in plasma insulin/ glucose ratio, and increased in isolated pancreatic islets the secretory responsiveness of the B-cell to D-glucose, but not carbamylcholine. These findings suggest that C-fibres may participate to the perturbation of glucose homeostasis in the diabetic Goto-Kakizaki rats.
Capsaicin
Pancreatic Islets
Insulin oscillation
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Decreased Pituitary Growth Hormone Content in Rats Treated Neonatally with High Doses of L-Thyroxine
Growth hormone and thyrotrophic hormone content have been measured by specific radioimmunoassays in anterior pituitaries of 22 day old rats. These animals were injected with saline or very high doses of L-thyroxine during the neonatal period in order to induce the "neo-T4" syndrome. Growth of such animals is known to be affected. It was found that not only TSH but also GH content of the T4-treated animals was significantly lower than that of the saline-injected controls.
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The effects of chronic neonatal hyperthyroidism in rats on the ontogenic pattern of serum corticosterone and growth hormone (GH) were studied. Thyroxine (T4) treated and saline injected rat pups were sacrificed under basal and stress conditions. In comparison to saline control animals, daily T4 administration (0.4 micrograms/gram body weight) produced a sustained elevation in basal corticosterone levels by day 12 and a significant elevation of serum corticosterone in response to stress by day 4. The serum GH levels in non-stressed animals were moderately decreased in response to T4 administration as compared to saline injected animals with a greater reduction in GH measured in samples obtained from stressed animals. The results indicate that chronic T4 administration influences the developmental pattern of serum corticosterone and GH under both non-stress and stress conditions.
Corticosterone
Basal (medicine)
Chronic Stress
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The adrenal glands of intact male rats fed a high sodium diet have a normal content of corticosterone and a low content of aldosterone. A low sodium diet is associated with a reduction of corticosterone and a marked increase in aldosterone. Chronic angiotensin treatment which has been previously shown to stimulate secretion of aldosterone and corticosterone is ineffective in the presence of a high sodium diet. Dietary sodium plays a significant role in the response of the rat adrenal to angiotensin. (Endocrinology84: 462, 1969)
Corticosterone
Mineralocorticoid
Low sodium diet
Low sodium
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The studies reported herein were conducted to confirm that the pituitary gland is involved in maintaining growth hormone (GH) resistance in rats with insulin-dependent diabetes mellitus (IDDM) and to determine whether the adrenocorticotropic hormone (ACTH)-adrenal cortical axis is responsible. The rats were made diabetic by injecting streptozotocin (85 mg/kg body wt) IP once daily on two consecutive days. They were then injected with 15 IU Insulin SC twice daily on two consecutive days to enable them to survive hypophysectomy or adrenalectomy. Intact nondiabetic (NonDb), diabetic (Db), hypophysectomized diabetic (HxDb), and adrenalectomized diabetic (AxDb) rats were injected twice daily with 50 μg porcine (p) GH or with 0.9% saline for 2 weeks following the surgeries. Serum glucose levels of the saline-injected Db, HxDb, and AxDb rats were significantly greater than those of the NonDb rats by 106%, 65% and 49%, respectively. However, the levels in the HxDb and AxDb animals were significantly lower than those of the Db group by 20% and 28%, respectively. Injections of pGH into NonDb rats increased serum glucose concentrations by 38%, over their saline-treated controls, and by 29% in AxDb rats. This diabetogenic effect of GH was not seen in any other group. Administration of pGH to Db rats failed to increase body weight gain, tail growth, tibial epiphysial plate width, or serum IGF-I concentration over saline-injected controls. By contrast, HxDb and AxDb rats injected with pGH showed significant increases in all four growth parameters. Total serum IGF-I concentrations in AxDb rats injected with pGH equaled those in NonDb controls. To determine whether the lack of corticosterone (B) in the AxDb rats was responsible for the reduced hyperglycemia and restored responsiveness to pGH, AxDb rats were given B in their drinking water at 5 or 25 μg/ml. Administration of B reduced the beneficial effects of adrenalectomy by restoring hyperglycemia and growth impairment, and partially restored resistance to the pGH injections. These studies confirm that the pituitary contributes to diabetic growth impairment and show that the ACTH-adrenal cortical axis is primarily responsible for the GH-resistant state that develops in rats with IDDM.
Hypophysectomy
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The changes in the levels of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) in the neurointermediate lobe of the pituitary (NIL) following hypertonic saline administration were examined in rats. The plasma osmotic pressure in rats receiving 2% NaCl for 8 days was greatly increased. Plasma AVP concentration in rats receiving 2% NaCl for 8 days were significantly higher than in control rats (566% of the control level). Plasma corticosterone was significantly higher in the saline-treated rats than in controls, whereas plasma ACTH was not significantly different. The pituitary ACTH concentration was much higher in the saline-treated rats than in controls. CRH in the NIL was increased significantly by saline treatment (419% of the control concentration), whereas the CRH in the paraventricular nucleus and median eminence of control and saline-treated rats did not differ significantly. The AVP in the NIL fell greatly in saline treated rats. The extract from both control and saline-treated rats showed a major peak for immunoreactive CRH, with a retention time identical to that of rat CRH. However, the peak was much higher in the extract from saline-treated rats. The immunoreactive AVP peak was greatly reduced in saline-treated rats. These results suggest that hypertonic saline administration increases the CRH in the NIL and causes AVP hypersecretion and/or hyperfunction of magnocellular-NIL CRH might be responsible for pituitary-adrenal stimulation in saline-treated rats.
Hypertonic saline
Median eminence
Corticosterone
Corticotropin-releasing hormone
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Objective : It has earlier been demonstrated that capsaicin-induced desensitization improves insulin sensitivity in normal rats. However, whether increased capsaicin-sensitive nerve activity precedes the onset of insulin resistance in diet-induced obesity – and therefore might be involved in the pathophysiology – is not known. Further, it is of relevance to investigate whether capsaicin desensitization improves glycaemic control even in obese individuals and we therefore chose the obese Zucker rats to test this. Design and methods : Plasma levels of calcitonin gene-related peptide (CGRP; a marker of sensory nerve activity) was assessed in 8-week-old Zucker rats. To investigate whether capsaicin desensitization (100 mg/kg at 9 weeks of age) would also ameliorate glycaemia in this non-diabetic model, we assessed oral glucose tolerance at 7 weeks after capsaicin. Results : It was found that plasma CGRP levels were elevated in obese Zucker rats prior to the onset of obesity (16.1±3.4 pmol/l in pre-obese Zucker rats vs 6.9±1.1 pmol/l in lean littermates; P = 0.015) despite similar body weights. Furthermore, capsaicin desensitization reduced both fasting blood glucose (4.3±0.2 mmol/l vs 5.1±0.2 mmol/l in controls; P = 0.050) as well as the mean blood glucose level during an oral glucose tolerance test (OGTT) (6.8±0.3 mmol/l vs 8.6±0.5 mmol/l in control obese rats; P = 0.024) whereas the plasma insulin levels during the OGTT were unchanged. However this did not lead to an improvement in insulin resistance or to a reduction of tissue triglyceride accumulation in muscle or liver. Conclusion : We concluded that capsaicin-induced sensory nerve desensitization improves glucose tolerance in Zucker rats. Since, in this study, plasma CGRP levels, a marker of sensory nerve activity, were increased in the pre-obese rats, our data support the hypothesis that increased activity of sensory nerves precedes the development of obesity and insulin resistance in Zucker rats.
Capsaicin
Hyperinsulinemia
Sensory nerve
Glucose tolerance test
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The effect of N-acetylserotonin (NAS) on serum levels of thyroid-stimulating hormone (TSH) in the male rat was investigated. In the first experiment, NAS and carrier were injected intraperitoneally into rats. The animals were sacrificed 30 and 60 min after injection. It was found that NAS (100 micrograms/rat) significantly depressed serum TSH 60 Min after injection when compared with saline-injected controls. In another experiment in which samples were obtained from rats at 0, 30, 60, 90 and 120 min after injection, significant decrease in serum TSH was observed at all time intervals after NAS (100 micrograms/rat) injection while no such difference was observed in the saline-injected groups. It is suggested that NAS may exert an inhibitory effect on TSH secretion.
Thyroid-stimulating hormone
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