Lactoferrin has a wide range of functions, and varied mechanisms of action.  Because of this, lactoferrin may offer solutions for metabolic diseases and their risk factors.

Metabolic Syndrome is, by definition, a combination of different risk factors that favour the development of severe, chronic diseases. At least three out of the five risk factors below must be present for a diagnosis of Metabolic Syndrome [1]:

  • Waist circumference > 88 cm (women), or > 102 cm (men)
  • Fasting blood glucose of more than 100 mg/dl
  • Fasting triglycerides of more than 150 mg/dl
  • HDL of less than 40 mg/dl (women), or less than 50 mg/dl (men)
  • Blood pressure reading over 130/85 mmHg

Interestingly, lactoferrin with its multiple functions can influence individual components of Metabolic Syndrome.  One of these is the regulation of carbohydrate and fat metabolism.  Lactoferrin can have a positive impact on the development of insulin resistance and high blood pressure, as well as on the formation of fat cells, inflammatory processes and other endocrine factors [2].

It has been shown that lactoferrin was able to reduce lipid peroxidation present with high cholesterol levels, significantly reducing the resultant oxidative stress [3].

The accumulation of visceral fat is one of the risk factors for Metabolic Syndrome.  It promotes the development of insulin resistance associated with high blood sugar levels, high blood pressure and problems with fat metabolism (dyslipidaemia).  The influence of lactoferrin on fat metabolism, and specifically on the formation of visceral fat, was investigated in a study by Ono, et al. [4].

In this double-blind placebo-controlled study, overweight male & female participants were given 300 mg of lactoferrin daily, over a period of eight weeks.

After the eight weeks, a significant reduction in the visceral fat quantity was measured.

In addition, participants were able to significantly reduce their body weight, body mass index (BMI) and hip circumference.

Based on the findings of various animal studies, the underlying mechanism is thought to be the ability of lactoferrin to bind lipopolysaccharides [5].  The inhibitory effect of lactoferrin on the maturation of fat cells (adipocytes) has also been examined [5,6]. Hofmann et al. describe how lactoferrin regulates the transport of fat into the visceral fat cells, thus blocking postprandial (after eating) fat uptake [7].

The study described above by Ono et al. showed that lactoferrin, without additional lifestyle changes, can reduce visceral fat [4]. And, as in other human studies, without any undesirable side effects.

A promising direction for further research and innovative therapeutic approaches.


1       Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002; 106: 3143–3421.

2       Elizarova A. Y., Kostevich V. A., Voynova I. V., Sokolov A. V. Lactoferrin as a promising remedy for metabolic syndrome therapy: from molecular mechanisms to clinical trials. Medical academic journal 2019; 19: 46–64.

3       Faridvand Y, Nozari S, Asoudeh-Fard A, Karimi M-A, Pezeshkian M, Safaie N, Nouri M. Bovine lactoferrin ameliorates antioxidant esterase activity and 8-isoprostane levels in high-cholesterol-diet fed rats. International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vitaminologie et de nutrition 2017; 87: 201–206.

4       Ono T, Murakoshi M, Suzuki N, Iida N, Ohdera M, Iigo M, Yoshida T, Sugiyama K, Nishino H. Potent anti-obesity effect of enteric-coated lactoferrin: decrease in visceral fat accumulation in Japanese men and women with abdominal obesity after 8-week administration of enteric-coated lactoferrin tablets. The British journal of nutrition 2010; 104: 1688–1695.

5       Moreno-Navarrete JM, Ortega FJ, Bassols J, Ricart W, Fernández-Real JM. Decreased circulating lactoferrin in insulin resistance and altered glucose tolerance as a possible marker of neutrophil dysfunction in type 2 diabetes. The Journal of clinical endocrinology and metabolism 2009; 94: 4036–4044.

6       Yagi M, Suzuki N, Takayama T, Arisue M, Kodama T, Yoda Y, Numasaki H, Otsuka K, Ito K. Lactoferrin suppress the adipogenic differentiation of MC3T3-G2/PA6 cells. Journal of oral science 2008; 50: 419–425.

7       Hofmann SM, Zhou L, Perez-Tilve D, Greer T, Grant E, Wancata L, Thomas A, Pfluger PT, Basford JE, Gilham D, Herz J, Tschöp MH, Hui DY. Adipocyte LDL receptor-related protein-1 expression modulates postprandial lipid transport and glucose homeostasis in mice. The Journal of clinical investigation 2007; 117: 3271–3282.