Hormonal and Metabolic Disorders of Human Immunodeficiency Virus Infection and Substance Abuse

Khalsa, Jag H.; Vocci, Frank; Dobs, Adrian S.

doi:10.3844/ajidsp.2006.125.129

Cited by 4 publications

(1 citation statement)

References 10 publications

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“…Moreover, leptin can possibly increase endothelin-1 expression and elevated levels of this peptide have been reported in numerous disease states including congestive heart failure, obesity and diabetes (Sakr, 2010). Research suggests that adipose tissue-derived hormones, adiponectin and/or leptin, may be playing an important role in energy homeostasis and insulin resistance in the HIV-associated metabolic syndrome (Khalsa et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Effect of Niacin on Hyperleptinemia and <i>Ob</i> Gene mRNA Over-Expression in Adipose Tissue of Dexamethasone Treated Rats

Shomali¹

2011

American Journal of Pharmacology and Toxicology

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Problem statement: Glucocorticoid-induced ob gene over-expression and resulted hyperleptinemia may lead to adverse consequences especially on cardiovascular system; therefore, the present study was conducted to evaluate the effects of niacin on hyperleptinemia and ob gene overexpression due to dexamethasone administration in rats. Approach: Twenty four adult male rats divided randomly into four equal groups: 1-normal saline (control), 2-dexamathasone 0.125 mg kg −1 day −1 , I.M. 3dexamathasone 0.125 mg kg −1 day −1 , I.M. + niacin 200 mg kg −1 day −1 , by oral gavages and 4-niacin 200 mg kg −1 day −1 , by oral gavages. After two weeks, blood samples were collected from all animals and leptin level assayed in harvested sera by ELISA method. Moreover, inguinal adipose tissue was excised to be examined for ob gene expression using quantitative real-time PCR. Results: Dexamethasone treatment (group 2) increased serum leptin along with its mRNA expression more than 3 folds as compared to control (p<0.001 and p = 0.001 respectively). Although leptin level in rats treated with dexamethasone+niacin was 17.8% lower than group 2; however this decrease was not significant (p>0.05). Concomitant administration of niacin with dexamethasone significantly decreased leptin gene mRNA expression compared to dexamethasone treated rats (p<0.001) and even reversed it to the control level (p>0.05). Niacin alone (group 4) had no effect on serum leptin concentration as well as leptin gene expression in comparison with control group (p>0.05). Conclusion: Niacin slightly ameliorates hyperleptinemia and reverses ob gene mRNA over-expression in adipose tissue of dexamethasone treated rats.

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Section: Introductionmentioning

confidence: 99%

Effect of Niacin on Hyperleptinemia and <i>Ob</i> Gene mRNA Over-Expression in Adipose Tissue of Dexamethasone Treated Rats

Shomali¹

2011

American Journal of Pharmacology and Toxicology

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HIV-1 clade C infection and progressive disruption in the relationship between cortisol, DHEAS and CD4 cell numbers: A two-year follow-up study

Chittiprol

Kumar

Shetty

et al. 2009

Clinica Chimica Acta

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Background It is well established that there is mutual interaction between the neuroendocrines and immune systems and that the disturbance in any one system could affect the function of the other. While there is a large body of evidence suggesting negative impact of human immunodeficiency virus type 1 B (HIV-1B) infection on both immune and neuroendocrine systems, the consequence of HIV-1 clade C infection (with structural differences from HIV-1B virus) on these systems is not clearly understood. Methods We carried out a 2-y longitudinal study on plasma profile of adrenocorticosteroids, including cortisol and DHEAS and their relationship with declining CD4+ cell counts in neurologically asymptomatic HIV-C infected individuals (N=84) in order to understand the impact of HIV-1 clade C infection on adrenocortical dysfunction and its relationship with the progressive decline in the cell mediated immunity. Results We found that while plasma cortisol levels increased significantly at baseline in HIV-1C infected individuals compared to those in HIV-negative controls (HIV-1C+, 9.83±0.39 vs. controls, 8.04±0.45; p< 0.01), there was a significant decrease in DHEAS in HIV-1C+ individuals, compared to that in HIV-negative controls (81.02 ± 4.9 vs. 185.1±12.03, p< 0.001), and consequently a significant increase in cortisol:DHEAS (Cortisol:DHEAS) ratio in HIV-1 clade C infected persons (0.19±0.002 vs. control 0.058±0.006; p<.0.001). Moreover, in HIV-1 C infected individuals, there was a strong positive correlation between DHEAS and CD4 cells (r=0.2; p<0.05), and a strong negative correlation between cortisol, as well as Cortisol:DHEAS ratio and CD4 cells (r= −0.25; p<0.01; and r= −0.31; p<0.001, respectively). Conclusions These findings suggest the persistent and progressive adrenocorical dysfunction during the asymptomatic phase of HIV infection, and that the evaluation of increase in plasma cortisol, a decrease in DHEAS, and an increase in Cortisol:DHEAS ratio may serve as important biomarkers preceding the impending down regulation of CD4 cell counts and progressive decline in the immune system function in HIV-1C infection. Furthermore, these findings may indicate the dysregulation of 3β-hydroxysteroid dehydrogenase (3β-HSD) activity, the enzyme involved in the biosynthesis of cortisol and DHEA through the pregnenolone-progesterone pathway, and that it may offer an opportunity for drug discovery targeting re-regulation of 3β-HSD activity for potential therapeutic application in HIV-1 C infection.

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γ-Linolenic Acid Prevents Lipid Metabolism Disorder in Palmitic Acid-Treated Alpha Mouse Liver-12 Cells by Balancing Autophagy and Apoptosis via the LKB1-AMPK-mTOR Pathway

Liang

Zhang

et al. 2021

J. Agric. Food Chem.

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Excessive fat deposition is the main character in nonalcoholic fatty liver disease (NAFLD), while γ-linolenic acid (GLA) is a polyunsaturated fatty acid that can reduce lipid deposition. This study investigated the effect and regulatory mechanism of GLA (100 μM) on lipid metabolism in alpha mouse liver 12 (AML-12) cells treated by 400 μM palmitic acid (PA). GLA reduced lipid content and increased fatty acid β oxidation, as indicated by decreasing triglyceride and cholesterol contents and increasing mRNA and protein expressions of CPT1α and PPARα. GLA relieved oxidative stress caused by PA, upregulated mRNA levels of superoxide dismutase and glutathione peroxidase, and decreased reactive oxygen species content. GLA reduced apoptosis, as indicated by decreases in the BAX/BCL2 expression level and apoptosis percentage. GLA activated autophagy, autophagosome-lysosome fusion, and LKB1-AMPK-mTOR signaling and upregulated mRNA and protein expressions of Beclin-1, autophagy-related 5, and liver kinase B1 (LKB1). These effects of GLA on lipid metabolism disorders of PA-treated hepatocytes were reversed by autophagy inhibitor 3MA and AMPK inhibitor compound C, confirming our conclusions. Overall, GLA can protect AML-12 cells from lipid metabolism disorder caused by PA via balancing autophagy and apoptosis mediated by the LKB1-AMPK-mTOR pathway. Consequently, GLA, as a dietary supplement, can help to prevent and treat NAFLD by regulating lipid metabolism and autophagy.

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Hormonal and Metabolic Disorders of Human Immunodeficiency Virus Infection and Substance Abuse

Cited by 4 publications

References 10 publications

Effect of Niacin on Hyperleptinemia and <i>Ob</i> Gene mRNA Over-Expression in Adipose Tissue of Dexamethasone Treated Rats

Effect of Niacin on Hyperleptinemia and <i>Ob</i> Gene mRNA Over-Expression in Adipose Tissue of Dexamethasone Treated Rats

HIV-1 clade C infection and progressive disruption in the relationship between cortisol, DHEAS and CD4 cell numbers: A two-year follow-up study

γ-Linolenic Acid Prevents Lipid Metabolism Disorder in Palmitic Acid-Treated Alpha Mouse Liver-12 Cells by Balancing Autophagy and Apoptosis via the LKB1-AMPK-mTOR Pathway

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