Soy protein intake prevents adipocyte hypertrophy in rats fed a high fat diet

Soy protein intake is known to cause microbiota changes. While there are some reports about the effect of soy protein intake on gut microbiota and lipid metabolism, effective timing of soy protein intake has not been investigated. In this study, we examined the effect of soy protein intake timing on microbiota. Mice were fed twice a day, in the morning and evening, to compare the effect of soy protein intake in the morning with that in the evening. Mice were divided into three groups: mice fed only casein protein, mice fed soy protein in the morning, and mice fed soy protein in the evening under high-fat diet conditions. They were kept under the experimental condition for two weeks and were sacrificed afterward. We measured cecal pH and collected cecal contents and feces. Short-chain fatty acids (SCFAs) from cecal contents were measured by gas chromatography. The microbiota was analyzed by sequencing 16S rRNA genes from feces. Soy protein intake whether in the morning or evening led to a greater microbiota diversity and a decrease in cecal pH resulting from SCFA production compared to casein intake. In addition, these effects were relatively stronger by morning soy protein intake. Therefore, soy protein intake in the morning may have relatively stronger effects on microbiota than that in the evening.

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Soy protein is beneficial but high-fat diet and voluntary running are detrimental to bone structure in mice

Nutrition Research ◽

10.1016/j.nutres.2015.04.012 ◽

2015 ◽

Vol 35 (6) ◽

pp. 523-531 ◽

Cited By ~ 9

Author(s):

Lin Yan ◽

George L. Graef ◽

Forrest H. Nielsen ◽

LuAnn K. Johnson ◽

Jay Cao

Keyword(s):

Soy Protein ◽

High Fat Diet ◽

Bone Structure ◽

High Fat ◽

Voluntary Running

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PPARγ Mediates High-Fat Diet–Induced Adipocyte Hypertrophy and Insulin Resistance

Molecular Cell ◽

10.1016/s1097-2765(00)80210-5 ◽

1999 ◽

Vol 4 (4) ◽

pp. 597-609 ◽

Cited By ~ 965

Author(s):

Naoto Kubota ◽

Yasuo Terauchi ◽

Hiroshi Miki ◽

Hiroyuki Tamemoto ◽

Toshimasa Yamauchi ◽

...

Keyword(s):

Insulin Resistance ◽

High Fat Diet ◽

High Fat ◽

Adipocyte Hypertrophy

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Effects of balanced deep-sea water on adipocyte hypertrophy and liver steatosis in high-fat, diet-induced obese mice

Obesity ◽

10.1002/oby.20740 ◽

2014 ◽

Vol 22 (7) ◽

pp. 1669-1678 ◽

Cited By ~ 21

Author(s):

Byung Geun Ha ◽

Jung-Eun Park ◽

Eun Ji Shin ◽

Yun Hee Shon

Keyword(s):

Deep Sea ◽

High Fat Diet ◽

Sea Water ◽

Liver Steatosis ◽

Obese Mice ◽

High Fat ◽

Deep Sea Water ◽

Adipocyte Hypertrophy

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Macadamia Oil Supplementation Attenuates Inflammation and Adipocyte Hypertrophy in Obese Mice

Mediators of Inflammation ◽

10.1155/2014/870634 ◽

2014 ◽

Vol 2014 ◽

pp. 1-9 ◽

Cited By ~ 11

Author(s):

Edson A. Lima ◽

Loreana S. Silveira ◽

Laureane N. Masi ◽

Amanda R. Crisma ◽

Mariana R. Davanso ◽

...

Keyword(s):

Adipose Tissue ◽

Insulin Sensitivity ◽

Lipid Profile ◽

High Fat Diet ◽

Control Diet ◽

Saturated Fatty Acids ◽

Peritoneal Macrophages ◽

High Fat ◽

Obesity In Mice ◽

Adipocyte Hypertrophy

Excess of saturated fatty acids in the diet has been associated with obesity, leading to systemic disruption of insulin signaling, glucose intolerance, and inflammation. Macadamia oil administration has been shown to improve lipid profile in humans. We evaluated the effect of macadamia oil supplementation on insulin sensitivity, inflammation, lipid profile, and adipocyte size in high-fat diet (HF) induced obesity in mice. C57BL/6 male mice (8 weeks) were divided into four groups: (a) control diet (CD), (b) HF, (c) CD supplemented with macadamia oil by gavage at 2 g/Kg of body weight, three times per week, for 12 weeks (CD + MO), and (d) HF diet supplemented with macadamia oil (HF + MO). CD and HF mice were supplemented with water. HF mice showed hypercholesterolemia and decreased insulin sensitivity as also previously shown. HF induced inflammation in adipose tissue and peritoneal macrophages, as well as adipocyte hypertrophy. Macadamia oil supplementation attenuated hypertrophy of adipocytes and inflammation in the adipose tissue and macrophages.

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Soy Protein Isolate Inhibits High-Fat Diet-Induced Senescence Pathways in Osteoblasts to Maintain Bone Acquisition in Male Rats

Endocrinology ◽

10.1210/en.2014-1427 ◽

2014 ◽

Vol 156 (2) ◽

pp. 475-487 ◽

Cited By ~ 19

Author(s):

Jin-Ran Chen ◽

Oxana P. Lazarenko ◽

Michael L. Blackburn ◽

Thomas M. Badger ◽

Martin J. J. Ronis

Keyword(s):

Signaling Pathways ◽

Soy Protein ◽

High Fat Diet ◽

Soy Protein Isolate ◽

Protein Isolate ◽

Cell Senescence ◽

Male Rats ◽

Osteoblastic Cells ◽

High Fat ◽

Caveolin 1

Chronic consumption by experimental animals of a typical Western diet high in saturated fats and cholesterol during postnatal life has been demonstrated to impair skeletal development. However, the underlying mechanism by which high-fat, energy-dense diets affect bone-forming cell phenotypes is poorly understood. Here, we show that male weanling rats fed a diet containing 45% fat and 0.5% cholesterol made with casein (HF-Cas) for 6 weeks displayed lower bone mineral density and strength compared with those of AIN-93G–fed dietary controls. Substitution of casein with soy protein isolate (SPI) in the high-fat diet (HF-SPI) prevented these effects. The bone-sparing effects of SPI were associated with prevention of HF-Cas–induced osteoblast senescence pathways through suppression of the p53/p21 signaling pathways. HF-Cas–fed rats had increased caveolin-1 and down-regulated Sirt1, leading to activations of peroxisome proliferator–activated receptor γ (PPARγ) and p53/p21, whereas rats fed HF-SPI suppressed caveolin-1 and activated Sirt1 to deacetylate PPARγ and p53 in bone. Treatment of osteoblastic cells with nonesterified free fatty acid (NEFA) increased cell senescence signaling pathways. Isoflavones significantly blocked activations of senescence-associated β-galactosidase and PPARγ/p53/p21 by NEFA. Finally, replicative senescent osteoblastic cells and bone marrow mesenchymal ST2 cells exhibited behavior similar to that of cells treated with NEFA and in vivo bone cells in rats fed the HF-Cas diet. These results suggest that (1) high concentrations of NEFA occurring with HF intake are mediators of osteoblast cell senescence leading to impairment of bone development and acquisition and (2) the molecular mechanisms underlying the SPI-protective effects involve isoflavone-induced inhibition of osteoblastic cell senescence to prevent HF-induced bone impairments.

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