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Anti-metabolic Syndrome Effect of Lactoferrin 
  
Increases in Basal Metabolic Rate and Bursts Fat Burning 1)
  
Obese people tend to have a low body temperature. Dr. Hiroshi Kimoto at Nagatsukai-Saitou Hospital has discovered the anti-metabolic syndrome effect of lactoferrin. The basal body temperature in control subjects is around 35.5 oC; these subjects are considered to have mild hypothermia. After a meal, most healthy individuals showed transient temperature elevation. The control subjects also showed transient temperature elevation; however, the elevation was picture6.GIF
relatively mild. Individuals that were administered 300 mg/day of enteric lactoferrin showed elevation of the basal body temperature as well as normal temperature after a meal. Enteric lactoferrin increases the basal metabolic rate and bursts the elevation of body temperature.
 
Reduction in intra-abdominal visceral fat of up to 40% within 60 days 2)
 

The accumulation of intra-abdominal visceral fat is inevitable in patients with metabolic syndrome. Lion Corporation has reported that enteric lactoferrin drastically reduced accumulated intra-abdominal visceral fat in individuals. For 2 months, 12 individuals (age range, 35.65 years) have consumed

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enteric lactoferrin (dosage, 300 mg/day). On an average, 20% of the area of intra-abdominal visceral fat was reduced, and the size of the waist also decreased by 4% on an average. In 1 case, 40% of the area of intra-abdominal visceral fat was reduced. Metabolic syndrome is a group of risk factors associated with obesity; these factors increase the risk of health problems such as heart disease and diabetes. The term "metabolic" refers to the biochemical processes involved in the normal functioning of the body. Risk factors are behaviors or conditions that increase the possibility of acquiring a disease. About 47 million adults in the United States (i.e., almost 25% of the population) have metabolic syndrome, and the number continues to increase. The figure shows the average abdominal fat area (left) and average waist size (right) of a total of 12 volunteers, including 8 men and 4 women. The abdominal fat area is calculated from a CT scan (images at the bottom).

 

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Reference
1) Milk Science 53 313-314 2004
2) Lion ,Corporate press release , March 19, 2007
 

   

Anti-aging Effects of Lactoferrin

 

Reactive Oxygen Species Promotes Aging

 

Aging is the accumulation of changes in organisms, such as the appearance of wrinkles and mottled skin. Oxygen and radical oxygen species are the key risk factors for aging. Molecular dioxygen (O2) is essential for cellular respiration in all aerobic organisms. In the mitochondria, oxygen is used to generate adenosine triphosphate (ATP) during oxidative phosphorylation. In the absence of oxygen supply, the

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individual suffers brain death within 5 minutes, and the heart stops beating within 10.20 minutes. Although oxygen is essential for energy production, its by-product is harmful to cells. During the process of mitochondrial energy production, a very low but significant amount of the hydroxyl radical (OH.) is produced. The hydroxyl radical is highly reactive, and it attacks any compound immediately after it is produced.

 

Lactoferrin fights against geriatric disorders

  

The oxidation of DNA and lipids is the major factor responsible for degenerative disorders of aging such as weakened muscles, immune-system decline, cancer, The antioxidative effect of lactoferrin When L-ascorbic acid and iron ammonium sulfate are added to egg-yolk phospholipid liposomes, the phospholipid is rapidly peroxidized. Lactoferrin inhibited cardiovascular

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disease, Alzheimer disease, and neurodegenerative disorder. Recently, it has been reported that lactoferrin is a potent antioxidant of DNA and lipids.

 

Antioxidant for lipids

 

In Fenton's reaction, the addition of catalysts, namely, Fe2+ and Cu+, markedly promoted hydroxyl radical production in the cell environment. Lactoferrin effectively scavenges thoseexcess ions from the cell environment and inhibits Fenton's cycling that is responsible for hydroxyl radical production.

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Antioxidant for DNA 1)

 

The hydroxyl radical occasionally oxidizes nuclear and mitochondrial DNA. Oral administration of lactoferrin in Long-Evans cinnamon rats (an animal model of Wilson disease) resulted in reduced 8-hydroxy-2Œ-deoxyguanosine (8-OHdG) in mitochondrial DNA extracted from the

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liver. 8-OHdG is a DNA base modified by the hydroxyl radical and is known to be an oxidative stress marker.

 

Reference
1) J. Hepatol. 48 486-493 2008

 

Antianxiety and Antinociceptive Effect of Lactoferrin

 

Transfer through the Blood-Brain Barrier 1)

 

A research group at Tottri University has reported that the concentration of lactoferrin in the cerebrospinal fluid of neonates of the miniature pig was markedly increased after the administration of colostrum. Although the blood-brain barrier (BBB) separates the circulating blood and cerebrospinal fluid, orally administered lactoferrin is effectively transferred from the blood to the cerebrospinal fluid. Interestingly, the rate of transportation is further increased in postweaning growth and not in the neonate. Lactoferrin is one of the very few proteins that can effectively pass through the BBB.

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Lactoferrin Enhances Antinociception 2)

 

It has been reported that lactoferrin enhances the effect of endogenous opioid. Endogenous opioids are naturally occurring peptides in the brain, such as endorphins and enkephalins. The antinociceptive effect of lactoferrin was reversed by naloxon, which is a K-opioid receptor antagonist. The antinociceptive effect of lactoferrin is mainly mediated by the K-opioid receptor. In addition to enhancing the effect of endogenous opioid, lactoferrin enhances the effect of morphine by 50.100 fold. Lactoferrin was also found to retard the development of resistance to morphine. Lactoferrin can be used in the treatment of terminal care in cancer patients to improve their quality of life and in the treatment of stress-related disorders in most individuals in urban areas.

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Reference
1) J Vet Med A Physiol Pathol Clin Med. 49 358-364 2002
2) Brain Res. 965 239-245 2003