Williams E.A.J.,Orthopaedics and Pharmacology Physiology |
Douard V.,Orthopaedics and Pharmacology Physiology |
Bajaj D.,Orthopaedics and Pharmacology Physiology |
Sabbagh Y.,Orthopaedics and Pharmacology Physiology |
And 2 more authors.
Proceedings of the IEEE Annual Northeast Bioengineering Conference, NEBEC | Year: 2013
High fructose (HF) intake is a public health problem. However, little is known about effects on bone quality during growth. Greater data exists for low calcium (Ca2+). We fed low-Ca (0.02%) and calorie-equivalent glucose and fructose diets (43%) to male, 3-wk-old, B6 mice for 5 wks. Four groups (n=9/group) were fed combinations of normal/low Ca and glucose/fructose. Weight and long-bone lengths were not affected. Consistent with literature, low-Ca diet resulted in less stiff and strong (∼40%; p65% (p20%, p<0.01) long bone and increased toughness (energy absorption) of longbone mid-shaft, measured by 3-point bending; post-yield displacement was increased in low Ca by >65% (p<0.05). By histomorphometry, low Ca resulted in decreased (>20%, p<0.05) cortical width, partially explaining the bending results. Only the glucose-fed group exhibited compensation to maintain outside circumference and diameter by increased periosteal bone formation rate (p.BFR); 3-fold greater vs. each of the other 3 groups (p<0.05). One plausible mechanism for poor circumferential growth involves bone in a feedback loop and is suggested by decreased intestinal Ca transport and Ca transporter protein in mucosa. The fructose diet completely prevented both adaptive increases in Ca transport, and 1α-hydroxylase-mediated synthesis of 1,25(OH)2D3 levels. © 2013 IEEE.