No abstract

The purpose of this study was to examine the effectiveness of collagen peptide intake on bone metabolism in growing (G) and calcium-deficient mature (M) rats. As for the dosages used, they were amounts equal to the recommended supplements for humans (0.166 g/kg body weight (BW) per day: Coll-1G and Coll-1M groups), 10-fold higher (1.66 g/kg BW per day: Coll-10G and Coll-10M groups), and 100-fold higher (16.6 g/kg BW per day: Coll-100G group). In growing male rats, bone mineral density (BMD) of the femur in the Coll-100G group was significantly higher than that in the other groups after the 4-week experimental period. On the other hand, kidneys in the rats from the Coll-100G group exhibited hypertrophy. To examine the effects of collagen peptide on bone metabolism in a calcium-deficient status, mature female rats were fed a 0.01% Ca diet for 9 weeks and then fed a diet with 0.2% calcium with or without collagen peptide (control, Coll-1M, and Coll-10M groups) or a 0.5% calcium diet (normal Ca) for 8 weeks. BMD of the whole femur in the Coll-10M group was significantly higher than that in the control and Coll-1M groups, and the level was similar to that in the normal Ca group. BMD of the lumbar spine in the Coll-10M group was significantly higher than their baseline value, as well as being significantly higher than that in the control and Coll-1M groups. These results suggest that orally administered collagen peptide may provide beneficial effects on bone metabolism, especially in the calcium-deficient condition, without obvious undesirable effects.

Soybean isoflavones have structures similar to that of estrogen and have received attention as alternatives to hormone replacement therapy for the prevention of postmenopausal osteoporosis. Daidzein, a major isoflavone found in soybean, is metabolized to equol by gut microflora, and the metabolite exhibits a stronger estrogenic activity than daidzein. However, there is no direct evidence that equol affects bone metabolism. In this study, we examined the effect of equol on the inhibition of bone loss in ovariectomized (OVX) mice. Female mice (8 wk old) were assigned to 5 groups as follows: sham-operated (sham), OVX, OVX + 0.1 mg/d equol administration (0.1 Eq), OVX + 0.5 mg/d equol administration (0.5 Eq), and OVX + 0.03 microg/d 17beta-estradiol administration (E(2)). Equol and E(2) were administered s.c., using a mini-osmotic pump. At 4 wk after the intervention, uterine weight was less in the OVX mice than in sham-operated mice (P < 0.05). The weight was maintained in the E(2) group. In contrast, administration of equol at doses used in this study did not affect uterine atrophy in OVX mice. Bone mineral density (BMD) for the whole body in the OVX group measured by dual-energy X-ray absorptiometry was lower than that in the sham group, whereas administration of 0.5 mg/d Eq as well as E(2) maintained the BMD. The BMD of the femur and lumbar spine in the OVX group was also lower than those in the sham group, and treatment with 0.5 mg/d Eq maintained it. Notably, the BMD of the proximal femur in the 0.5 Eq group was the same as that of the sham group. E(2) inhibited bone loss from all regions induced by OVX. These results suggest that equol, a major metabolite of daidzein, inhibits bone loss apparently without estrogenic activity in the reproductive organs of OVX mice.

Fushiki (2014) Unsaturated long-chain fatty acids inhibit the binding of oxidized low-density lipoproteins to a model CD36, Bioscience, Biotechnology, and Biochemistry, 78:2, 238-244,

CD36 is an integral membrane protein that mediates the cellular uptake of oxidized low-density lipoprotein (oxLDL) through recognition of the oxidized glycerophospholipids (oxPLs) formed during LDL oxidation. We aimed to devise an assay system to detect binding between CD36 and oxLDL/oxPL without using recombinant proteins. A peptide corresponding to amino-acid residues 149-168 of mouse CD36 with biotin at its N-terminus (named biotin-CD36(149-168)) and variants of it were synthesized and immobilized onto streptavidin-coated plates. oxLDL labeled with Alexa-Fluor-488 bound specifically and saturably to immobilized biotin-CD36(149-168), but poorly or not at all to the variants, such as that with a scrambled amino-acid sequence. The binding of fluorescence-labeled oxLDL to biotin-CD36(149-168) was inhibited efficiently by an oxPL species, but not by a nonoxidized glycerophospholipid. This assay system using biotin-CD36(149-168) provides a convenient means not only of characterizing binding profiles between CD36 and oxLDL/oxPL but also of finding competitors for the binding.