This study used 1H nuclear magnetic resonance (NMR) spectroscopy to examine the metabolic profiles of plasma and urine from the low-density lipoprotein receptors (LDLR) knockout mice.
Consistent with previous studies, these mice developed hypercholesterolemia and atherosclerosis when fed a high-fat/cholesterol/cholate containing diet. In addition, multivariate statistical analysis of the metabolomic data highlighted significant differences in tricarboxylic acid cycle and fatty acid metabolism, as a result of high-fat/cholesterol diet feeding. The high-fat/cholesterol/cholate diet, LDL receptor gene deficiency, and the diet-genotype interaction caused a significant perturbation in choline metabolism, notably the choline oxidation pathway. Specifically, the loss in the LDL receptor caused a marked reduction in the urinary excretion of betaine and dimethylglycine, especially when the mice are fed a high fat/cholesterol/cholate diet.
These metabolic changes are comparable with those detected in ApoE knockout mice fed the same high-fat/cholesterol/cholate diet and may be useful for monitoring the onset of atherosclerosis across animal models.
Cheng et al (2010). "A metabolomic study of the LDL receptor null mouse fed a high-fat diet reveals profound perturbations in choline metabolism that are shared with ApoE null mice." Physiol. Genomics 41: 224-231.
Sunday, April 4, 2010
Betaine improves adipose function in high fat diet
This study examined the effects of betaine supplementation on hepatic fat accumulation and injury in mice fed high-fat diet and evaluated mechanisms underlying its hepatoprotective effects.
Male C57BL/6 mice weighing 25 {+/-} 0.5 g (means {+/-} SE) were divided into four groups (8 mice per group) and started on one of four treatments: control diet (Con), control diet supplemented with betaine (BT), high-fat diet (HF), and high-fat diet supplemented with betaine (HB). Betaine was supplemented in the drinking water at a concentration of 1% (wt/vol) (anhydrous).
Long-term high-fat feeding caused NAFLD in mice, which was manifested by excessive neutral fat accumulation in the liver and elevated plasma ALT levels. Betaine supplementation alleviated hepatic pathological changes, which were concomitant with attenuated insulin resistance as shown by improved HOMA-IR values and glucose tolerance test (GTT), and corrected abnormal adipokine (adiponectin, resistin, and leptin) productions. In specific, betaine supplementation enhanced insulin sensitivity in adipose tissue as shown by improved ERK1/2 and Akt activations. In adipocytes freshly isolated from mice fed high-fat diet, pretreatment of betaine enhanced insulin signaling pathway and improved adipokine productions. Further investigation using whole liver tissues revealed that betaine supplementation alleviated high-fat diet induced endoplasmic reticulum (ER) stress response in adipose tissue as shown by attenuated GRP78/CHOP protein abundance and JNK activation.
The findings suggest that betaine might serve as a safe and efficacious therapeutic tool for NAFLD by improving adipose tissue function.
Wang et al (2010). "Betaine Improved Adipose Tissue Function in Mice Fed High-Fat Diet: A Mechanism for Hepatoprotective Effect of Betaine in Non-alcoholic Fatty Liver Disease." Am J Physiol Gastrointest Liver Physiol 298: G634-G642
Male C57BL/6 mice weighing 25 {+/-} 0.5 g (means {+/-} SE) were divided into four groups (8 mice per group) and started on one of four treatments: control diet (Con), control diet supplemented with betaine (BT), high-fat diet (HF), and high-fat diet supplemented with betaine (HB). Betaine was supplemented in the drinking water at a concentration of 1% (wt/vol) (anhydrous).
Long-term high-fat feeding caused NAFLD in mice, which was manifested by excessive neutral fat accumulation in the liver and elevated plasma ALT levels. Betaine supplementation alleviated hepatic pathological changes, which were concomitant with attenuated insulin resistance as shown by improved HOMA-IR values and glucose tolerance test (GTT), and corrected abnormal adipokine (adiponectin, resistin, and leptin) productions. In specific, betaine supplementation enhanced insulin sensitivity in adipose tissue as shown by improved ERK1/2 and Akt activations. In adipocytes freshly isolated from mice fed high-fat diet, pretreatment of betaine enhanced insulin signaling pathway and improved adipokine productions. Further investigation using whole liver tissues revealed that betaine supplementation alleviated high-fat diet induced endoplasmic reticulum (ER) stress response in adipose tissue as shown by attenuated GRP78/CHOP protein abundance and JNK activation.
The findings suggest that betaine might serve as a safe and efficacious therapeutic tool for NAFLD by improving adipose tissue function.
Wang et al (2010). "Betaine Improved Adipose Tissue Function in Mice Fed High-Fat Diet: A Mechanism for Hepatoprotective Effect of Betaine in Non-alcoholic Fatty Liver Disease." Am J Physiol Gastrointest Liver Physiol 298: G634-G642
Determinants of total homocysteine concentration
This study assessed the association between choline and betaine intakes and fasting and post-methionine-load homocysteine concentrations using the USDA revised food-composition tables and evaluated whether the associations varied by folic acid fortification periods in 1325 male and 1407 female participants in the sixth examination (1995-1998) of the Framingham Offspring Study.
A higher choline-plus-betaine intake was associated with lower concentrations of post-methionine-load homocysteine. They found an inverse association between choline-plus-betaine intake and fasting homocysteine concentrations. When stratified by plasma folate and vitamin B-12 concentrations, the inverse association was limited to participants with low plasma folate or vitamin B-12 concentrations. In the postfortification period, the inverse association between choline-plus-betaine intake and either fasting or post-methionine-load homocysteine was no longer present.
Choline and betaine intakes were associated with both fasting and post-methionine-load total homocysteine concentrations, especially in participants with low folate and vitamin B-12 status. The inverse association between choline and betaine intakes and homocysteine concentrations was no longer present in the postfortification period.
Lee et al (2010). "Are dietary choline and betaine intakes determinants of total homocysteine concentration?" Am J Clin Nutr 91(5) 1303-10
A higher choline-plus-betaine intake was associated with lower concentrations of post-methionine-load homocysteine. They found an inverse association between choline-plus-betaine intake and fasting homocysteine concentrations. When stratified by plasma folate and vitamin B-12 concentrations, the inverse association was limited to participants with low plasma folate or vitamin B-12 concentrations. In the postfortification period, the inverse association between choline-plus-betaine intake and either fasting or post-methionine-load homocysteine was no longer present.
Choline and betaine intakes were associated with both fasting and post-methionine-load total homocysteine concentrations, especially in participants with low folate and vitamin B-12 status. The inverse association between choline and betaine intakes and homocysteine concentrations was no longer present in the postfortification period.
Lee et al (2010). "Are dietary choline and betaine intakes determinants of total homocysteine concentration?" Am J Clin Nutr 91(5) 1303-10
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