Pneumosepsis survival in the setting of obesity leads to persistent steatohepatitis and metabolic dysfunction.

Background: As critical care practice evolves, the sepsis survivor population continues to expand, often with lingering inflammation in many organs, including the liver. Given the concurrently increasing population of patients with NAFLD, in this study, we aimed to understand the long-term effect of sepsis on pre-existing NAFLD and hyperglycemia.

Methods: Male mice were randomized to a high-fat diet or a control diet (CD).

Bacoside A downregulates matrix metalloproteinases 2 and 9 in DEN-induced hepatocellular carcinoma.

Cancer metastasis is a complex multi-step process, responsible for a majority of cancer-related deaths by affecting the critical organs and causing complications in therapies. Hepatocellular carcinoma is a multi-factorial disease and is the third most common cause of cancer related mortality worldwide. Clinical and experimental studies have shown that MMP-2 and MMP-9 are involved in tumor invasion and metastases and their elevated expression has been associated with poor prognosis.

Chemopreventive effect of bacoside A on N-nitrosodiethylamine-induced hepatocarcinogenesis in rats.

Purpose: Chemoprevention is an effective approach to control hepatocarcinogenesis. Bacoside A, the active constituent of Bacopa monniera Linn., is anticipated to play a role in chemoprevention of liver cancer.

Studies on hypoglycaemic effects of polyherbal preparation in streptozotocin-induced diabetic male albino rats.

Many traditional treatments have been recommended in the alternative system of medicine for diabetes mellitus. However, the mode of action of most of the herbals used has not been defined. It has been reported that sex hormones are important regulators of insulin-mediated events in skeletal muscles.

Differential response of Leydig cells in expressing 11beta-HSD type I and cytochrome P450 aromatase in male rats subjected to corticosterone deficiency.

Emerging evidence suggests that the glucocorticoid and estradiol are important for Leydig cell steroidogenesis and are regulated via aromatase for estradiol production and 11beta-HSD for oxidatively inactivating glucocorticoid. Although it is known that corticosterone deficiency impaired Leydig cell steroidogenesis, its effect on the expression of Leydig cell 11beta-HSD type I and aromatase are yet to be recognized. Following metyrapone-induced corticosterone deficiency, serum corticosterone and testosterone levels decrease, whereas serum estradiol remains unaltered.

Sex steroids enhance insulin receptors and glucose oxidation in Chang liver cells.

Background: The present study was designed to assess the effect of sex steroids (testosterone and 17beta-estradiol) on insulin receptor expression, insulin binding and glucose oxidation in human liver cell line.

Methods: Non-malignant Chang liver cells were treated with different concentrations of testosterone and 17beta-estradiol dissolved in serum free medium for 24 h to identify the effective dose of both steroids for further studies. Cells with 70-80% confluency were challenged with testosterone (0.

Hepatoprotective activity of bacoside A against N-nitrosodiethylamine-induced liver toxicity in adult rats.

N-Nitrosodiethylamine (DEN) is a notorious carcinogen, present in many environmental factors. DEN induces oxidative stress and cellular injury due to enhanced generation of reactive oxygen species; free radical scavengers protect the membranes from DEN-induced damage. The present study was designed to evaluate the protective effect of bacoside A (the active principle isolated from Bacopa monniera Linn.

Effects of corticosterone deficiency and its replacement on Leydig cell steroidogenesis.

Clinical and experimental studies have shown the adverse effects of glucocorticoid deficiency/metyrapone treatment on testicular Leydig cell testosterone production. However, molecular mechanisms that underlie the effects of glucocorticoid deficiency on Leydig cell steroidogenesis are not yet determined. Therefore, the present study was designed to assess the mechanism of this phenomenon.

Differential effect of corticosterone deficiency on the expression of LH, prolactin and insulin receptors on rat Leydig cells.

The adverse effects of glucocorticoid deficiency on the expression of genes encoding Leydig cell surface receptors and the response to LH/prolactin/insulin to produce testosterone production are yet to be recognized. Following metyrapone-induced corticosterone deficiency, serum corticosterone, testosterone and insulin levels decrease, whereas serum prolactin exhibits a significant increase and serum LH remains unaltered. LH binding and LH receptor mRNA expression were not altered, but a significant decrease in PRL and insulin binding and in the mRNA expressions of their receptors were observed in corticosterone-deficient rats in vivo.

Assessment of in vitro effects of metyrapone on Leydig cell steroidogenesis.

Metyrapone, a specific inhibitor of 11beta-hydroxylase inhibits glucocorticoid production and it is used in the diagnosis/treatment of hypercortisolism and also to test the functional integrity of hypothalamo-pituitary-adrenal axis. To assess the impact of glucocorticoid deficiency, this drug is preferred over adrenalectomy, which eliminates all the hormonal secretions of the adrenal cortex and medulla. However, whether metyrapone has any direct effect on the extra-adrenocortical cellular or tissue functions remains to be resolved.

Diethylhexyl phthalate impairs insulin binding and glucose oxidation in Chang liver cells.

The present study examined the dose-dependent effects of diethylhexyl phthalate (DEHP) on insulin receptor concentration and glucose oxidation in Chang liver cells. Chang liver cells (5 x 10(5) cells) were exposed to different concentrations (0, 50, 100, 200 and 400 microM) of DEHP for 24h. At the end of exposure, cells were utilized for assessing insulin receptor concentration and glucose oxidation.

Effects of excess corticosterone on NADPH generating enzymes and glucose oxidation in Leydig cells of adult rats.

Clinical and experimental studies have shown the adverse effects of excess glucocorticoid on testicular testosterone production. The NADPH co-enzyme has been recognized as an important factor that regulates several steps in steroidogenesis, while glucose oxidation acts as a limiting factor on testicular testosterone production. Nevertheless, the impact of excess corticosterone, the stress hormone on testicular NADPH availability and glucose oxidation is unknown.

Metyrapone-induced corticosterone deficiency impairs glucose oxidation and steroidogenesis in Leydig cells of adult albino rats.

The present study was designed to identify the effects of metyrapone-induced corticosterone deficiency on Leydig cell steroidogenesis in adult male rats. Adult Wistar rats (200-250 g body weight) were treated with metyrapone, an inhibitor of corticosterone synthesis (10 mg/100 g body weight, s.c.