Obesity leads to changes in the gut microbial community which contribute to the metabolic dysregulation in obesity. Dietary fat and fiber affect the caloric density of foods. The impact of dietary fat content and fiber type on the microbial community in the hind gut is unknown. Effect of dietary fat level and fiber type on hindgut microbiota and volatile fatty acid (VFA) profiles was investigated. Expression of metabolic marker genes in the gut, adipose tissue and liver was determined. A 2 × 2 experiment was conducted in pigs fed at two dietary fat levels (5% or 17.5% swine grease) and two fiber types (4% inulin, fermentable fructo-oligosaccharide or 4% solka floc, non-fermentable cellulose). High fat diets (HFD) resulted in a higher (P<0.05) total body weight gain, feed efficiency and back fat accumulation than the low fat diet. Feeding of inulin, but not solka floc, attenuated (P<0.05) the HFD-induced higher body weight gain and fat mass accumulation. Inulin feeding tended to lead to higher total VFA production in the cecum and resulted in a higher (P<0.05) expression of acyl coA oxidase (ACO), a marker of peroxisomal β-oxidation. Inulin feeding also resulted in lower expression of sterol regulatory element binding protein 1c (SREBP-1c), a marker of lipid anabolism. Bacteria community structure characterized by DGGE analysis of PCR amplified 16S rRNA gene fragments showed that inulin feeding resulted in greater bacterial population richness than solka floc feeding. Cluster analysis of pairwise Dice similarity comparisons of the DGGE profiles showed grouping by fiber type but not the level of dietary fat. Canonical correspondence analysis (CCA) of PCR- DGGE profiles showed that inulin feeding negatively correlated with back fat thickness. This study suggests a strong interplay between dietary fat level and fiber type in determining susceptibility to obesity.
Obesity during pregnancy predisposes offspring to metabolic diseases such as obesity and diabetes. Few studies have explored the molecular underpinnings of the increased obesity risk in the offspring. To determine the effects of excessive maternal energy intake on adiposity in the offspring, pregnant Duroc x Landrace gilts were fed either a normal energy (mNE) or high energy diet (mHE) to induce excessive pregnancy weight gain. Offspring were sacrificed at 48h after birth and at weaning (day 21). Expression of adipogenic genes was measured using RT‐PCR. Expression of genes such as PPARγ and CEBPα was not different between mNE and mHE offspring at 48h after birth, but they were induced (P < 0.05) in mHE offspring at weaning. Additionally, SFRP4, SFRP5 and PAI‐1 were induced in mHE offspring at weaning. However, SRC1 expression was higher in mNE offspring at 48h, but not different at weaning (P < 0.05). The expression of PPARγ corepressors, SIRT1 and NCoR1, was elevated (P < 0.05) in mHE offspring at weaning. Therefore, excessive maternal energy intake during gestation programs offspring for increased adiposity through induction of adipogenic transcription factors and suppression of wnt signaling. Grant Funding Source : Showalter Research Trust
Many pregnancies in the United States result in weight gain in excess of recommendations. Few data exist on the impact of maternal weight gain on offspring despite evidence demonstrating that early life environment precipitates risks for metabolic syndrome. Excessive gestation weight gain and postnatal diet were assessed using a swine model of human health. Offspring from Landrace x Duroc gilts fed a normal (mNE) or a high energy diet (mHE) to induce a 30% increase in gestation weight gain were weaned to either a normal (wNE) or high energy (wHE) diet. At 3 months of age piglets fed wHE had increased (P < 0.05) backfat compared with wNE and suppressed (P < 0.05) hepatic and intestine (1.51 vs. 0.48 and 0.85 vs. 0.47, respectively for wNE vs. wHE) PEPCK‐C abundance. Intestine PGC‐1α abundance was significantly lower in offspring from mHE gilts (0.94 vs. 0.60 for mNE vs. mHE). Offspring from mHE gilts weaned onto a wHE diet had elevated (P < 0.05) blood glucose (102 vs. 64 mg/dl), insulin (0.10 vs. 0.21 ng/ml) and lower NEFAs (0.62 vs. 0.31 mmol/L) compared to mHEwNE offspring. Postnatal wHE did not induce the same metabolic perturbations in the mNE offspring (GLU 70 vs. 80 mg/dl, ILN 0.16 vs. 0.13 mg/dl, NEFA 0.43 vs. 0.43 mmol/L for mNEwNE vs. mNEwHE). These data show gestational weight gain of 30% in excess of recommendations and a nutrient‐rich postnatal environment precipitate indications of metabolic syndrome. Grant Funding Source : Showalter Trust Fund
Abstract Background Soy oil is a major vegetable oil consumed in the US. A recently developed soybean variety produces oil with a lower concentration of α-linolenic acid, hence a higher (n-6)/(n-3) ratio, than regular soy oil. The study was conducted to determine the metabolic impact of the low α-linolenic acid containing soy oil. Methods Ossabaw pigs were fed diets supplemented with either 13% regular soybean oil (SBO), or 13% of the low α-linolenic soybean oil (LLO) or a control diet (CON) without extra oil supplementation, for 8 weeks. Results Serum and adipose tissue α-linolenic acid concentration was higher in pigs fed the SBO diet than those on the CON and LLO diets. In the serum, the concentration of saturated fatty acids (SFA) was lower in the LLO group than in CON and SBO groups polyunsaturated fatty acid (PUFA) concentration was higher in the LLO group compared to CON and SBO groups. Glucose, insulin, triglycerides and LDL-cholesterol were higher in pigs fed the SBO diet than those fed the CON and LLO diets. HDL-cholesterol was lower in pigs on the SBO diet than those on the CON and LLO diets. Pigs fed SBO and LLO diets had lower CRP concentration than those on the CON diet. Adipose tissue expression of Interleukin 6 (IL-6) was higher in the SBO and LLO diets than the CON. Expression of ECM genes, COLVIA and fibronectin, was significantly reduced in the SBO diet relative to the CON and LLO diets whereas expression of inflammation-related genes, cluster of differentiation 68 (CD68) and monocyte chemoattractant protein 1 (MCP-1), was not different across treatments. Conclusions Results suggest that lowering the content of α-linolenic acid in the context of a high fat diet could lead to mitigation of development of hyperinsulinemia and dyslipidemia without significant effects on adipose tissue inflammation.
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