Regression Models of Magnesium Intake on Insulin Resistance.

1<p>Regression model adjusted for caloric intake, physical activity, medication use and menopausal status.</p>2<p>β = Unstandardized Beta (standard error), β* = Standardized Beta (standard error), Magnesium intake (g/day/kg).</p>3<p>Normal-weight, overweight and obese groups are based upon %BF according to the Bray criteria (25).</p>4<p>Magnesium intake (Pre-Menopause 360.63±209.8 mg/day, Post-Menopause 353.82±192.9 mg/day) (Entire cohort, Normal-weight, Overweight, & Obese – See Table.1).</p>5<p>Statistical significance was set to p<0.05 (IBM SPSS Statistics 19).</p

Physical, Biochemical, and Dietary Intake Characteristics of Normal-weight, Overweight, and Obese Participants.

1<p>Data presented as mean ± SD. Homeostasis model assessment of insulin resistance (HOMA-IR) and β-cell function (HOMA-β). Gender differences were assessed with a one-way ANOVA. Subjects were also stratified into normal-weight, overweight and obese based upon %BF according to the Bray criteria (25). Adiposity differences were assessed with an ANCOVA controlling for caloric intake, physical activity, medication use, and menopause. ²Significantly greater for men compared to women. ³Significantly greater for women compared to men. ⁴Statistical significance for one-way ANOVA and ANCOVA were set to p<0.05 (IBM SPSS Statistics 19).</p

Regression Models of Magnesium Intake on Insulin Resistance based upon %BF and BMI.

1<p>Regression model adjusted for caloric intake, physical activity, medication use and menopausal status.Subjects were also stratified into a tertiles(Low, Medium and High) based upon %BF and BMI.</p>2<p>β = Unstandardized Beta (standard error), β* = Standardized Beta (standard error), Magnesium intake (g/day/kg).</p>3<p>Magnesium intake (Low BMI 409.78±243.5 mg/day, Medium BMI 353.24±180.9 mg/day, High BMI 342.76±196.1 mg/day) (Low %BF 387.5±230.3 mg/day, Medium %BF 360.54±187.5 mg/day, High %BF 357.68±210.7 mg/day).</p>4<p>Statistical significance was set to p<0.05 (IBM SPSS Statistics 19).</p

Physical, Biochemical, and Dietary Intake Characteristics According to Magnesium Intake.

1<p>Data presented as mean ± SD. Homeostasis model assessment of insulin resistance (HOMA-IR) and β-cell function (HOMA-β).</p>2<p>Subjects were stratified into a tertile (low, medium and high) based upon magnesium intake (mg/day).</p>3<p>Magnesium intake group differences were assessed with an ANCOVA controlling for caloric intake, physical activity, medication use, menopause and %BF.</p>4<p>Statistical significance for one-way ANCOVA was set to p<0.05 (IBM SPSS Statistics 19).</p

Lysophosphatidic acid receptor mRNA levels in heart and white adipose tissue are associated with obesity in mice and humans

<div><p>Background</p><p>Lysophosphatidic acid (LPA) receptor signaling has been implicated in cardiovascular and obesity-related metabolic disease. However, the distribution and regulation of LPA receptors in the myocardium and adipose tissue remain unclear.</p><p>Objectives</p><p>This study aimed to characterize the mRNA expression of LPA receptors (LPA1-6) in the murine and human myocardium and adipose tissue, and its regulation in response to obesity.</p><p>Methods</p><p>LPA receptor mRNA levels were determined by qPCR in i) heart ventricles, isolated cardiomyocytes, and perigonadal adipose tissue from chow or high fat-high sucrose (HFHS)-fed male C57BL/6 mice, ii) 3T3-L1 adipocytes and HL-1 cardiomyocytes under conditions mimicking gluco/lipotoxicity, and iii) human atrial and subcutaneous adipose tissue from non-obese, pre-obese, and obese cardiac surgery patients.</p><p>Results</p><p>LPA1-6 were expressed in myocardium and white adipose tissue from mice and humans, except for LPA3, which was undetectable in murine adipocytes and human adipose tissue. Obesity was associated with increased LPA4, LPA5 and/or LPA6 levels in mice ventricles and cardiomyocytes, HL-1 cells exposed to high palmitate, and human atrial tissue. LPA4 and LPA5 mRNA levels in human atrial tissue correlated with measures of obesity. LPA5 mRNA levels were increased in HFHS-fed mice and insulin resistant adipocytes, yet were reduced in adipose tissue from obese patients. LPA4, LPA5, and LPA6 mRNA levels in human adipose tissue were negatively associated with measures of obesity and cardiac surgery outcomes. This study suggests that obesity leads to marked changes in LPA receptor expression in the murine and human heart and white adipose tissue that may alter LPA receptor signaling during obesity.</p></div

Nutritional composition of research diets.

<p>Nutritional composition of research diets.</p

Patient characteristics and metabolic parameters.

<p>Patient characteristics and metabolic parameters.</p

Experimental design and groups for LPA receptor expression analysis.

<p>Experimental layout of LPA receptor mRNA quantification in A) heart and adipose tissue from non-obese, pre-obese, and obese cardiac surgery patients, B) heart, adipose tissue, and cardiomyocytes from lean and obese mice, C) insulin sensitive and insulin resistant 3T3-L1 adipocytes, and D) insulin sensitive and insulin resistant HL-1 cardiomyocytes.</p

LPA receptor mRNA levels in myocardial tissue and cells.

<p>A) LPA1-6 mRNA levels in ventricles from chow and HFHS-fed mice in fed and 16-h fasted states (n = 5). B) LPA1-6 mRNA levels in cardiomyocytes isolated from chow and HFHS-fed mice (n = 3). C) LPA1-6 mRNA levels in HL-1 cardiomyocytes incubated in the presence or absence of 1.2 mM palmitate for 16 h (n = 3). D) LPA1-6 mRNA levels in atrial tissue from non-obese, pre-obese, and obese patients undergoing cardiac surgery (n = 6 for non-obese and pre-obese, n = 18 for obese). A-D) *<i>P</i> < 0.05, **<i>P</i> < 0.01, ***<i>P</i> < 0.001 as determined using two-way ANOVA followed by a Tukey post hoc analysis (A, D) or unpaired two-tailed t-test (B, C).</p

Sequence information for primers employed in qPCR analysis.

<p>Sequence information for primers employed in qPCR analysis.</p