PLC restores the impaired responses to glucose overload and insulin administration induced by high-fat (HF) fed animals.

<p>A, B and C: Intraperitoneal glucose tolerance test performed in overnight fasted animals. A: Plasma glucose concentrations at baseline and at 30, 60, 90 and 120 minutes after glucose overload (2 mg/kg). B: Incremental glucose concentrations at 30, 60, 90 and 120 minutes after glucose overload. C: Area under curves describing the increase of glycaemia from 0 to 120 minutes after the glucose overload. D, E and F: Insulin sensitivity test. D. Plasma glucose concentrations at baseline and at 30, 60, 90 and 120 after insulin administration (0.8 U/kg body weight). E: Decrease of glycaemia suffered at 30, 60, 90 and 120 after insulin injection. F Area under curves describing the decrease of glycaemia from 0 to 120 minutes after the insulin administration. Values are means and SEM (n = 10). ^##<i>P</i><0.01, ^###<i>P</i><0.001 <i>vs</i> vehicle-ST, *<i>P</i><0.05 <i>vs</i> vehicle-HF.</p

PLC treatment improves activity of mitochondrial respiratory chain complexes.

<p>CS: citrate synthase. Enzymatic activities are expressed in nmol of product formed per min and per mg of protein. Values are means and SEM (n = 10).</p>#<p><i>P</i><0.05 <i>vs</i> vehicle-ST,</p>*<p><i>P</i><0.05 <i>vs</i> vehicle-HF.</p

PLC improves cardiac function.

<p>A: Left ventricular systolic end diameter. B: Left ventricular diastolic end diameter. C: Ejection fraction. D: Cardiac output. E: Cardiac index (cardiac output normalized to the animal body weight). F: Systolic blood pressure. Values are means and SEM (n = 10). ^###<i>P</i><0.001 <i>vs</i> vehicle-ST, *<i>P</i><0.05, **<i>P</i><0.01 <i>vs</i> vehicle-HF.</p

PLC increased the nitric oxide (NO) release in heart, skeletal muscle and aorta.

<p>Measurement of <i>in situ</i> NO production by electron paramagnetic resonance in skeletal muscle (A), aorta (B), heart (C) and liver (D). Values are means and SEM (n = 10). ^##<i>P</i><0.01, ^#<i>P</i><0.05 <i>vs</i> vehicle-ST, ***<i>P</i><0.001, *<i>P</i><0.05 <i>vs</i> vehicle-HF.</p

PLC exerts beneficial effects on different biochemical plasma parameters evaluating the presence of insulin resistance, the lipid profile and the free- and acyl-carnitines plasma levels.

<p>LC: L-carnitine; PLC: propionyl-l-carnitine; LC-AC: long-chain acylcarnitines. Values are means and SEM (n = 10).</p>#<p><i>P</i><0.05,</p>##<p><i>P</i><0.01,</p>###<p><i>P</i><0.001 <i>vs</i> vehicle-ST,</p>*<p><i>P</i><0.05,</p>**<p><i>P</i><0.01 and</p>***<p><i>P</i><0.001 <i>vs</i> vehicle-HF.</p

PLC treatment decreases high-fat (HF) diet-induced body weight gain without changing the food intake in mice with established diet-induced obesity (i.e. mice previously fed.

<p>A: Body weight increases during PLC treatment period (from 9^th to 14^th week). B: Daily food intake. Values are means and SEM (n = 10). ^##<i>P</i><0.01, ^###<i>P</i><0.001 <i>vs</i> vehicle-ST, **<i>P</i><0.01 <i>vs</i> vehicle-HF.</p

PLC improves high-fat (HF) diet-induced endothelial dysfunction.

<p>Concentration-response curves to acetylcholine (ACh, 1 nmol/l to 10 mmol/l) in the presence and in the absence of the nitric oxide synthase inhibitor N^ω-nitro-L-arginine-methyl ester (L-NAME 300 mmol/l). Values are means and SEM (n = 10). ^XXX<i>P</i><0.001 vs ACh in the absence of L-NAME, ^##<i>P</i><0.01 <i>vs</i> vehicle-ST, **<i>P</i><0.01, ***<i>P</i><0.001 <i>vs</i> vehicle-HF.</p

Additional file 1: of Association of environmental markers with childhood type 1 diabetes mellitus revealed by a long questionnaire on early life exposures and lifestyle in a case–control study

The questionnaire used in the current study. (PDF 620 kb