Downsizing Your Plate
We all know we should not overeat if we wish to manage our weight. However, that’s not always easy. I was brought up with my mother’s words such “you’re not leaving the table until your plate’s empty” and “eat up, you can’t waste food”. It’s not always easy to change old habits.

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Iron, Folate Supplements May Harm Kids in Regions Rife With Malaria (Healthday)
For years, health workers have distributed iron and folic acid supplements to malnourished children throughout the developing world, to help fight pediatric anemia. (more…)

AICAR inhibits adipocyte differentiation in 3T3L1 and restores metabolic alterations in diet-induced obesity mice model
Background:
Obesity is one of the principal causative factors involved in the development of metabolic syndrome. AMP-activated protein kinase (AMPK) is an energy sensor that regulates cellular metabolism. The role of AMP-activated protein kinase in adipocyte differentiation is not completely understood, therefore, we examined the effect of 5-aminoimidazole-4-carboxamide-1-?-D-ribofuranoside (AICAR), a pharmacological activator of AMP-activated protein kinase (AMPK) on adipocyte differentiation in 3T3L1 cells and in a mouse Diet induced obesity (DIO) model.
Methods:
To examine the effect of AICAR on adipocyte differentiation in 3T3L1 cells and in a mouse Diet induced obesity (DIO) model, 3T3L1 cells were differentiatied in the presence or absence of different concentration of AICAR and neutral lipid content and expression of various adipocyte-specific transcription factors were examined. In vivo study, treated and untreated mice with AICAR (0.1?0.5 mg/g body weight) were fed high-fat diet (60% kcal% fat) to induce DIO and several parameters were studied.
Results:
AICAR blocked adipogenic conversion in 3T3L1 cells along with significant decrease in the neutral lipid content by downregulating several adipocyte-specific transcription factors including peroxisome proliferators-activated receptor ? (PPAR?), C/EBP? and ADD1/SREBP1, which are critical for adipogenesis in vitro. Moreover, intraperitoneal administration of AICAR (0.5 mg g/body weight) to mice fed with high-fat diet (60% kcal% fat) to induce DIO, significantly blocked the body weight gain and total content of epididymal fat in these mice over a period of 6 weeks. AICAR treatment also restored normal adipokine levels and resulted in significant improvement in glucose tolerance and insulin sensitivity. The reduction in adipose tissue content in AICAR treated DIO mice was due to reduction in lipid accumulation in the pre-existing adipocytes. However, no change was observed in the expression of PPAR?, C/EBP? and ADD1/SREBP1 transcription factors in vivo though PGC1? expression was significantly induced.
Conclusion:
This study suggests that AICAR inhibits adipocyte differentiation via downregulation of expression of adipogenic factors in vitro and reduces adipose tissue content in DIO mice by activating expression of PGC1? without inhibiting adipocyte-specific transcription factors in DIO mice. (more…)

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Marginal vitamin C status is associated with reduced fat oxidation during submaximal exercise in young adults
Background:
Vitamin C is a cofactor in the biosynthesis of carnitine, a molecule required for the oxidation of fatty acids. A reduction in the ability to oxidize fat may contribute to the reported inverse relationship between vitamin C status and adiposity. To examine this possibility, we conducted a preliminary trial to evaluate the impact of vitamin C status on fat oxidation during submaximal exercise.
Methods:
Fat energy expenditure was determined in individuals with marginal (n = 15) or adequate (n = 7) vitamin C status during a submaximal, 60-minute treadmill test. Subsequently, eight of the subjects with marginal vitamin C status completed an 8-week double-blind, placebo-controlled, depletion-repletion trial with submaximal exercise testing.
Results:
Individuals with marginal vitamin C status oxidized 25% less fat per kg body weight during the treadmill test as compared to individuals with adequate vitamin C status. Fat oxidation during exercise was inversely related to fatigue (r = -0.611, p = 0.009). Vitamin C repletion of vitamin C depleted subjects (500 mg vitamin C/d) raised fat energy expenditure during exercise 4-fold as compared to depleted control subjects (p = 0.011).
Conclusion:
These preliminary results show that low vitamin C status is associated with reduced fat oxidation during submaximal exercise. Low vitamin C status may partially explain the inverse relationship between vitamin C status and adiposity and why some individuals are unsuccessful in their weight loss attempts. (more…)