Pancreatic insulin secretion in rats fed a soy protein high fat diet depends on the interaction between the amino acid pattern and isoflavones.
Obesity is frequently associated with the consumption of high carbohydrate/fat diets leading to hyperinsulinemia. We have demonstrated that soy protein (SP) reduces hyperinsulinemia, but it is unclear by which mechanism. Thus, the purpose of the present work was to establish whether SP stimulates insulin secretion to a lower extent and/or reduces insulin resistance, and to understand its molecular mechanism of action in pancreatic islets of rats with diet-induced obesity. Long-term consumption of SP in a high fat (HF) diet significantly decreased serum glucose, free fatty acids, leptin, and the insulin:glucagon ratio compared with animals fed a casein HF diet. Hyperglycemic clamps indicated that SP stimulated insulin secretion to a lower extent despite HF consumption. Furthermore, there was lower pancreatic islet area and insulin, SREBP-1, PPARgamma, and GLUT-2 mRNA abundance in comparison with rats fed the casein HF diet. Euglycemic-hyperinsulinemic clamps showed that the SP diet prevented insulin resistance despite consumption of a HF diet. Incubation of pancreatic islets with isoflavones reduced insulin secretion and expression of PPARgamma. Addition of amino acids resembling the plasma concentration of rats fed casein stimulated insulin secretion; a response that was reduced by the presence of isoflavones, whereas the amino acid pattern resembling the plasma concentration of rats fed SP barely stimulated insulin release. Infusion of isoflavones during the hyperglycemic clamps did not stimulate insulin secretion. Therefore, isoflavones as well as the amino acid pattern seen after SP consumption stimulated insulin secretion to a lower extent, decreasing PPARgamma, GLUT-2, and SREBP-1 expression, and ameliorating hyperinsulinemia observed during obesity.
Noriega-López
Lilia
L
Depto. de Fisiología de la Nutrición, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México, D.F. 14000, México.
Tovar
Armando R
AR
Gonzalez-Granillo
Marcela
M
Hernández-Pando
Rogelio
R
Escalante
Bruno
B
Santillán-Doherty
Patricio
P
Torres
Nimbe
N
D000596:Amino Acids / Q000494:pharmacology*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002364:Caseins / Q000008:administration & dosage / Q000009:adverse effects; D002478:Cells, Cultured; D004041:Dietary Fats / Q000008:administration & dosage* / Q000009:adverse effects; D004044:Dietary Proteins / Q000008:administration & dosage* / Q000009:adverse effects; D005786:Gene Expression Regulation / Q000187:drug effects; D005934:Glucagon / Q000097:blood; D015309:Glucose Clamp Technique; D051273:Glucose Transporter Type 2 / Q000096:biosynthesis; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood* / Q000209:etiology / Q000473:pathology; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism* / Q000473:pathology; D007529:Isoflavones / Q000494:pharmacology*; D020738:Leptin / Q000097:blood; D009765:Obesity / Q000097:blood* / Q000150:complications / Q000473:pathology; D047495:PPAR gamma / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D030262:Soybean Proteins / Q000009:adverse effects / Q000494:pharmacology*; D051780:Sterol Regulatory Element Binding Protein 1 / Q000096:biosynthesis
D000596:Amino Acids; D001786:Blood Glucose; D002364:Caseins; D004041:Dietary Fats; D004044:Dietary Proteins; D051273:Glucose Transporter Type 2; D007328:Insulin; D007529:Isoflavones; D020738:Leptin; D047495:PPAR gamma; C495683:Slc2a2 protein, rat; D030262:Soybean Proteins; C497389:Srebf1 protein, rat; D051780:Sterol Regulatory Element Binding Protein 1; D005934:Glucagon