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Magnesium as a regulator of hepatic ...

Voma, Chesinta B.

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Magnesium as a regulator of hepatic NADPH in the hepatocyte: Prospective roles of magnesium in diabetes and obesity onset.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Magnesium as a regulator of hepatic NADPH in the hepatocyte: Prospective roles of magnesium in diabetes and obesity onset./
Author:	Voma, Chesinta B.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2014,
Description:	130 p.
Notes:	Source: Dissertations Abstracts International, Volume: 76-07, Section: B.
Contained By:	Dissertations Abstracts International76-07B.
Subject:	Cellular biology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3671638
ISBN:	9781321487800

Magnesium as a regulator of hepatic NADPH in the hepatocyte: Prospective roles of magnesium in diabetes and obesity onset.
Voma, Chesinta B.

Magnesium as a regulator of hepatic NADPH in the hepatocyte: Prospective roles of magnesium in diabetes and obesity onset. - Ann Arbor : ProQuest Dissertations & Theses, 2014 - 130 p.

Source: Dissertations Abstracts International, Volume: 76-07, Section: B.

Thesis (Ph.D.)--Cleveland State University, 2014.

This item must not be sold to any third party vendors.

Clinically quantifiable liver functions take place within the hepatocytes (80% of liver cells). Magnesium (Mg2+) deficiency has been correlated with the onset and progression of diabetes, and obesity yet, no cause-effect relationship has been identified. The current western diet is approximately 35% deficient in Mg2+. The effect of Mg2+ deficiency on hormonal physiological control has not been fully elucidated. The principal reservoir of Mg2+ (i.e., the bone) is not readily exchangeable with circulating extracellular Mg 2+ , thus in Mg2+ deficiency, initial losses come from the extracellular space since equilibrium with bone stores does not begin for several weeks. Mg2+ is highly concentrated within the endoplasmic reticulum, 15-20 mmol/L [Mg2+]Total . H6PD, the reticular counterpart of the cytosolic G6PD, is the main NADPH generating enzyme within the endoplasmic reticulum of the hepatocyte and an ancillary enzyme in pre-receptor glucocorticoid activation. NADPH-dependent 11β-HSD1 generates cortisol from its inactive form cortisone, thus eliciting high intra-hepatic active glucocorticoid concentrations, which in turn affects hepatocyte metabolism and response to insulin. Previous research has focused on the sensing of carbon (mostly glucose) and nitrogen sources (mostly amino acids). This study tests the hypothesis that Mg 2+ depletion alters hepatic metabolism and hormonal response via an increased cortisol production, leading to the onset of obesity, insulin resistance, and diabetes. HepG2 cells were grown in the presence of 0.6 (deficient) or 1.0 mmol/L (physiological) [Mg2+ ]o and analyzed for NADPH and 11β-HSD1-mediated cortisol production. Additionally, H6PD, and 11β-HSD1 expression levels were analyzed by RT-PCR and Western Blot analysis together with other downstream products regulated by cortisol. Gluconeogenic genes also upregulated, include FOXO1,PEPCK, F16BP. Our results indicate that NADPH production increased by ∼60% in Mg2+ deficient cells, and resulted in approximately two fold increase in cortisol production. Also, Mg2+ deficient cells showed 3 to 4 fold increase in H6PD and 11β-HSD1 mRNA and protein expression. Overall, our results support the hypothesis that Mg2+ deficiency increases H6PD activity and expression, setting the conditions for increased production of cortisol, decreased insulin responsiveness, and increased gluconeogenesis within the hepatocytes.

ISBN: 9781321487800Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Diabetes

Magnesium as a regulator of hepatic NADPH in the hepatocyte: Prospective roles of magnesium in diabetes and obesity onset.
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300 $a 130 p.
500 $a Source: Dissertations Abstracts International, Volume: 76-07, Section: B.
500 $a Publisher info.: Dissertation/Thesis.
500 $a Advisor: Anderson, David;Romani, Andrea.
502 $a Thesis (Ph.D.)--Cleveland State University, 2014.
506 $a This item must not be sold to any third party vendors.
520 $a Clinically quantifiable liver functions take place within the hepatocytes (80% of liver cells). Magnesium (Mg2+) deficiency has been correlated with the onset and progression of diabetes, and obesity yet, no cause-effect relationship has been identified. The current western diet is approximately 35% deficient in Mg2+. The effect of Mg2+ deficiency on hormonal physiological control has not been fully elucidated. The principal reservoir of Mg2+ (i.e., the bone) is not readily exchangeable with circulating extracellular Mg 2+ , thus in Mg2+ deficiency, initial losses come from the extracellular space since equilibrium with bone stores does not begin for several weeks. Mg2+ is highly concentrated within the endoplasmic reticulum, 15-20 mmol/L [Mg2+]Total . H6PD, the reticular counterpart of the cytosolic G6PD, is the main NADPH generating enzyme within the endoplasmic reticulum of the hepatocyte and an ancillary enzyme in pre-receptor glucocorticoid activation. NADPH-dependent 11β-HSD1 generates cortisol from its inactive form cortisone, thus eliciting high intra-hepatic active glucocorticoid concentrations, which in turn affects hepatocyte metabolism and response to insulin. Previous research has focused on the sensing of carbon (mostly glucose) and nitrogen sources (mostly amino acids). This study tests the hypothesis that Mg 2+ depletion alters hepatic metabolism and hormonal response via an increased cortisol production, leading to the onset of obesity, insulin resistance, and diabetes. HepG2 cells were grown in the presence of 0.6 (deficient) or 1.0 mmol/L (physiological) [Mg2+ ]o and analyzed for NADPH and 11β-HSD1-mediated cortisol production. Additionally, H6PD, and 11β-HSD1 expression levels were analyzed by RT-PCR and Western Blot analysis together with other downstream products regulated by cortisol. Gluconeogenic genes also upregulated, include FOXO1,PEPCK, F16BP. Our results indicate that NADPH production increased by ∼60% in Mg2+ deficient cells, and resulted in approximately two fold increase in cortisol production. Also, Mg2+ deficient cells showed 3 to 4 fold increase in H6PD and 11β-HSD1 mRNA and protein expression. Overall, our results support the hypothesis that Mg2+ deficiency increases H6PD activity and expression, setting the conditions for increased production of cortisol, decreased insulin responsiveness, and increased gluconeogenesis within the hepatocytes.
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653 $a Magnesium
653 $a Nadph
653 $a Obesity
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