April 2016 – Vol. 10, Issue 4

 

In This Issue…
                                                                           

  • Can adiponectin – the fat burning hormone – be considered a cancer marker?
  • Magnesium reduces arterial stiffness
  • In vitro study sheds light on vitamin D’s anti-obesity effect
  • Carnitine may help blunt the effects of a high fat diet
  • Zinc supplementation may help open up blood vessels


CLINICAL UPDATE – Can adiponectin – the fat burning hormone – be considered a cancer marker?

Studies on adiponectin, a hormone produced in fat cells that helps regulate glucose metabolism, have been equivocal on its link to chronic disease.  Research links low adiponectin to diabetes, obesity and cancer while other studies link high adiponectin to increased mortality for several chronic diseases.  Recent research confirms that too little and too much adiponectin are both problematic.
In one study, adiponectin suppressed cells in breast tissue that contribute to the development of mestatic breast cancer, suggesting that adiponectin may be beneficial during a precancerous state. However, after cancer has developed, the relationship between adiponectin and cancer seems to change.  For example, colon cancer patients in the highest quartile of adiponectin levels had a much higher risk of dying than patients with the lowest adiponectin levels, leading researchers to conclude that “adiponectin may be a marker for cancers that develop through specific pathways that may be associated with worsened prognosis.” 
(Cancer Prevention Research, December 2015)
LINK to ABSTRACT Prediagnostic Plasma Adiponectin and Survival among Patients with Colorectal Cancer.
LINK to ABSTRACT Leptin and Adiponectin Modulate the Self-renewal of Normal Human Breast Epithelial Stem Cells.

 

 

CLINICAL UPDATE – Magnesium reduces arterial stiffness
In this randomized, double-blind, placebo-controlled trial, 53 overweight adults were given magnesium supplements three times daily (350 mg total per day) or placebo.  Arterial stiffness was measured (via carotid-to-femoral pulse wave velocity) at the beginning of the trial, after 12 weeks and again at 24 weeks.  After three months (12 weeks), neither serum magnesium nor arterial stiffness had changed in the supplemented group.  However, after 6 months (24 weeks), magnesium levels had increased in the supplemented group while arterial stiffness had significantly decreased, suggesting that the physiologic effects of supplementation – at least for magnesium – may not become apparent for several months.
(American Journal of Clinical Nutrition, April 2016)
LINK to ABSTRACT
 Long-term magnesium supplementation improves arterial stiffness in overweight and obese adults: results of a randomized, double-blind, placebo-controlled intervention trial.

 

 

CLINICAL UPDATE – In vitro study sheds light on vitamin D’s anti-obesity effect
Low levels of vitamin D have been linked to obesity in several studies and recent research helps shed light on a possible mechanism of action behind this clinical effect. When fat cells were treated directly with vitamin D, they tended to burn more intracellular fat molecules specifically by changing the metabolic rate and expression of enzymes involved in energy metabolism.  In addition, genes that promote beta-oxidation (raise cellular fat burning potential) increased in expression when exposed to vitamin D.
(Nutrition, December 2015)
LINK to ABSTRACT Vitamin D decreases adipocyte lipid storage and increases NAD-SIRT1 pathway in 3T3-L1 adipocytes.
LINK to FREE FULL TEXT

 

CLINICAL UPDATE – Carnitine may help blunt the effects of a high fat diet
For eight weeks, mice were fed a high fat diet and given a supplement of l-carnitine for the last four weeks. Fatty liver disease developed in all the mice during the high fat diet/ no carnitine phase of the experiment. When l-carnitine – an amino acid responsible for transporting fatty acids into the cell mitochondria for metabolism – was given, the fatty liver (hepatic steatosis) and liver cell damage was prevented even as the mice continued on the high fat diet.  Another effect of carnitine supplementation was that insulin receptors in the liver become more sensitized, leading to the conclusion that “supplementation of l-carnitine is a promising approach for prevention and treatment of metabolic syndrome-related nonalcoholic steatohepatitis.”
(Hepatology Research, April 2016)
LINK to ABSTRACT
 L-carnitine prevents metabolic steatohepatitis in obese diabetic KK-Ay mice.

 

 

CLINICAL UPDATE – Zinc supplementation may help open up blood vessels
In this animal study, one group of hamsters was fed fructose in their drinking water while another group of hamsters were given normal water.  In addition, some animals were given zinc supplements while others did not receive any zinc supplementation.  Specific tests that measure the animals’ blood vessel response when exposed to chemicals known to induce dilation of the blood vessels were performed.
The blood vessels of the animals given zinc were much more responsive to chemical cues to open up (dilate) than those not given zinc.  Furthermore, the zinc supplementation helped prevent permeability in the blood vessels that normally occurs when blood vessels are subjected to oxygen deprivation, leading researchers to conclude that “zinc supplementation can improve macrovascular dysfunction.”
(Nutrition Metabolism and Cardiovascular Disease, April 2016)
LINK to ABSTRACT
Microcirculatory effects of zinc on fructose-fed hamsters.