Dr. Hans-Joachim Gabius (Ludwig Maximilian University of Munich, Germany), was a great glycobiologist, dedicated educator and respected Editorial Organizer. He suddenly passed away on August 2, 2021 at the age of 66. We have had the honor to collaborate with Dr. Gabius on numerous occasions, including editorial meetings and international conferences, where we exchanged ideas and discussed the “sugar code” and galectins. Dr. Gabius had enthusiastically supported this series on the Glycoforum website, which focuses on galectins and the unsolved questions surrounding this field. He has shared with us his thoughts and profound insights on the evolution and molecular function of galectin. We were lost for words when learning of his passing, and are hit by a deep sense of loss and sadness. We were looking forward to asking Hans for a sequel of his original contribution entitled “Galectins: (much) more than ga(lactose-binding)lectins” published in February 2021, and have difficulty accepting the fact that we have lost such an extraordinary scientist. We sincerely hope that condolences given by members of this series can help to alleviate the grief of the bereaved family.
On behalf of the members of the Galectins series
Editors: Jun Hirabayashi (Tokai National Higher Education Organization Nagoya University, Institute for Glyco-core Research) and Sachiko Sato (Laval University School of Medicine, CHU de Quebec Research Center)
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The binding affinity of lectins for glycans is generally displayed at the µM level; however, milk contains more than 10 mM oligosaccharides and 100 mM lactose. Such an astonishingly high concentration of glycans present in milk could inhibit the binding of most endogenous lectins to their glycan ligands. Then, many questions naturally arise, for example: what is the biological significance of the inhibitory activity? How high are the milk oligosaccharide concentrations in the digestive tract, and what is the pharmacokinetics of milk oligosaccharides in the body?
In this spin-off version, we try to present our guesses or “daydream” – our extended speculation – and discuss about how milk oligosaccharides are used once they enter the body, what roles they may play, and what their relationship may be to the function of galectins, which are abundant in the digestive tract. In addition, we reconsider the reason why mammals have acquired the ability to biosynthesize lactose and use it as a nutrient source for babies, which is said to be the “key to the evolutionary success of mammals”. ...and more
Human milk contains 7% of carbohydrate, 80% of which consists of lactose (Galβ1-4Glc), while 20% consists of oligosaccharides. The concentrations of milk oligosaccharides are 12 ~ 13 g/L in mature milk and 22 ~ 24 g/L in colostrum1; these are the third largest solid component after lactose and lipid. Their concentrations are surprisingly high. Most of the human milk oligosaccharides (HMOs), with few exceptions, contain a lactose unit at their reducing ends, to which monosaccharides residues including N-acetylglucosamine (GlcNAc), galactose (Gal), fucose (Fuc), and N-acetylneuraminic acid (Neu5Ac) are attached. To date about 250 HMOs have been separated, of which about 170 structures have been characterized. When breast-fed infants consume their mothers’ milk, the lactose is hydrolyzed to Glc and Gal by small intestinal lactase, to be absorbed, whereas most HMOs remain intact within the small intestine and thus reach the colon, where they have significant physiological functions other than nutritional effects. Based on the experimental evidence, the following functions have been proposed: stimulation of the growth of beneficial colonic bacteria such as bifidobacterium, anti-infection against pathogenic bacteria and viruses, immune modulation including anti-inflammation, prevention of necrotizing enterocolitis and reinforcement of the colonic barrier function, and activation of brain-nerve functions. ...and more
Cardiovascular and cerebrovascular diseases such as myocardial and cerebral infarction are caused by atherosclerotic disease1. Atherosclerotic diseases are the cause of approximately 25% of deaths in Japan, and constitute a major threat to the Japanese population, so there is a very high societal demand for these diseases to be defeated.
Treatment of atherosclerosis has previously focused on controlling the risk factors for cardiovascular disease development, represented by hypertension, diabetes, dyslipidemia, etc. Various risk factors are in fact increasingly controllable with renin-angiotensin system inhibitors, statins, etc. However, taking into consideration the continuing increase in the prevalence of cardiovascular diseases, there is an urgent need to establish new treatment strategies. ...and more
