Anti-diabetic effects including diabetic nephropathy of anti-osteoporotic trace minerals on diabetic mice.
OBJECTIVE
In our previous study to evaluate the effects of soluble silicon (Si) on bone metabolism, Si and coral sand (CS) as a natural Si-containing material suppressed peroxisome proliferator-activated receptor γ (PPARγ), which regulates both glucose and bone metabolism and increases adipogenesis at the expense of osteogenesis, leading to bone loss. In this study, we investigated the anti-diabetic effects of bone-seeking elements, Si and stable strontium (Sr), and CS as a natural material containing these elements using obese diabetic KKAy mice.


METHODS
Weanling male mice were fed diets containing 1% Ca supplemented with CaCO(3) as the control and CS, and diets supplemented with 50 ppm Si or 750 ppm Sr to control diet for 56 d. The mRNA expressions related to energy expenditure in the pancreas and kidney were quantified by real-time polymerase chain reaction.


RESULTS
At the end of feeding, plasma glucose, insulin, leptin, and adiponectin levels decreased significantly in three test groups, while pancreatic PPARγ and adiponectin mRNA expression levels increased significantly toward the normal level, improving the glucose sensitivity of β-cells and inducing a significant decrease in insulin expression. The renal PPARγ, PPARα, and adiponectin expression levels, histologic indices of diabetic glomerulopathy, and plasma indices of renal function were also improved significantly in the test groups.


CONCLUSIONS
Taken together, anti-osteoporotic trace minerals, Si and Sr, and CS containing them showed novel anti-diabetic effects of lowering blood glucose level, improving the tolerance to insulin, leptin, and adiponectin, and reducing the risk of glomerulopathy through modulation of related gene expression in the pancreas and kidney.
Maehira
Fusako
F
Department of Biometabolic Chemistry, School of Health Sciences, Faculty of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan. fmaehira@med.u-ryukryu.ac.jp
Ishimine
Nau
N
Miyagi
Ikuko
I
Eguchi
Yukinori
Y
Shimada
Katsumasa
K
Kawaguchi
Daisuke
D
Oshiro
Yoshihide
Y
D052242:Adiponectin / Q000097:blood / Q000235:genetics / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D050071:Bone Density Conservation Agents; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D003928:Diabetic Nephropathies / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D019587:Dietary Supplements; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D007328:Insulin / Q000097:blood; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D007678:Kidney Glomerulus / Q000187:drug effects / Q000473:pathology; D020738:Leptin / Q000097:blood; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010024:Osteoporosis; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D020799:Pancrelipase / Q000378:metabolism; D012825:Silicon / Q000494:pharmacology / Q000627:therapeutic use*; D017655:Silicon Compounds / Q000494:pharmacology / Q000627:therapeutic use*; D012987:Soil / Q000737:chemistry; D014131:Trace Elements / Q000494:pharmacology / Q000627:therapeutic use*
D052242:Adiponectin; D015415:Biomarkers; D001786:Blood Glucose; D050071:Bone Density Conservation Agents; D007004:Hypoglycemic Agents; D007328:Insulin; D020738:Leptin; D047495:PPAR gamma; D017655:Silicon Compounds; D012987:Soil; D014131:Trace Elements; D020799:Pancrelipase; D012825:Silicon