Rats perinatally exposed to food restriction and high-fat diet show differences in adipose tissue gene expression under chronic caloric restriction

Mackay, Harry A.; Khazall, Rim; Patterson, Zachary R.; Wellman, Martin; Abizaid, Alfonso

doi:10.4161/adip.24752

Cited by 10 publications

(11 citation statements)

References 50 publications

(54 reference statements)

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“…Previous studies by us and others have demonstrated that adipose tissue is very vulnerable to the effects of developmental programming and is the site in which some of the earliest and most striking programming effects are observed (15, 30, 31). Consistent with these observations, in the current study, we have shown a reduction in IRS-1 and p110- β insulin signaling protein expression in response to suboptimal nutrition in utero and catch-up growth.…”

Section: Discussionmentioning

confidence: 96%

Coenzyme Q10 Prevents Insulin Signaling Dysregulation and Inflammation Prior to Development of Insulin Resistance in Male Offspring of a Rat Model of Poor Maternal Nutrition and Accelerated Postnatal Growth

et al. 2015

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Low birth weight and rapid postnatal growth increases the risk of developing insulin resistance and type 2 diabetes in later life. However, underlying mechanisms and potential intervention strategies are poorly defined. Here we demonstrate that male Wistar rats exposed to a low-protein diet in utero that had a low birth weight but then underwent postnatal catch-up growth (recuperated offspring) had reductions in the insulin signaling proteins p110-β (13% ± 6% of controls [P < .001]) and insulin receptor substrate-1 (39% ± 10% of controls [P < .05]) in adipose tissue. These changes were not accompanied by any change in expression of the corresponding mRNAs, suggesting posttranscriptional regulation. Recuperated animals displayed evidence of a proinflammatory phenotype of their adipose tissue with increased IL-6 (139% ± 8% [P < .05]) and IL1-β (154% ± 16% [P < .05]) that may contribute to the insulin signaling protein dysregulation. Postweaning dietary supplementation of recuperated animals with coenzyme Q (CoQ10) (1 mg/kg of body weight per day) prevented the programmed reduction in insulin receptor substrate-1 and p110-β and the programmed increased in IL-6. These findings suggest that postweaning CoQ10 supplementation has antiinflammatory properties and can prevent programmed changes in insulin-signaling protein expression. We conclude that CoQ10 supplementation represents an attractive intervention strategy to prevent the development of insulin resistance that results from suboptimal in utero nutrition.

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Section: Discussionmentioning

confidence: 96%

Coenzyme Q10 Prevents Insulin Signaling Dysregulation and Inflammation Prior to Development of Insulin Resistance in Male Offspring of a Rat Model of Poor Maternal Nutrition and Accelerated Postnatal Growth

et al. 2015

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“…On the other hand, animal studies have indicated the potential for BM to promote the transfer of obesity from mother to offspring ( Del Prado, Delgado & Villalpando, 1997 ; Mackay et al, 2013 ; Matsuno et al, 1999 ; Oosting et al, 2015 ; Palou et al, 2010 ; Sun et al, 2012 ; Tsuduki et al, 2013 ). The influence of factors within the BM, which could contribute to the maternal transfer of obesity, have rarely been studied.…”

Section: Introductionmentioning

confidence: 99%

The adipokine C1q TNF related protein 3 (CTRP3) is elevated in the breast milk of obese mothers

Kwon

Cress

Clark

et al. 2018

PeerJ

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BackgroundC1q TNF related protein 3 (CTRP3) is a relatively novel hormonal factor primarily derived from adipose tissue and has anti-diabetic properties. To determine if CTRP3 could play a role in early childhood development, the purpose of this study was to establish the presence of CTRP3 in breast milk (BM) and to determine whether CTRP3 levels were correlated with pregravid obesity status of the mother.MethodsBreast milk was collected from breast-feeding mothers who had a pregravid body mass index (BMI) classification of normal weight (BMI 18–25 kg/m2, n = 23) or obese (BMI > 30 kg/m2, n = 14). Immunoprecipitation followed by immunoblot analysis confirmed the presence of CTRP3 in BM. The concentration of CTRP3 in BM samples was determined by ELISA. Additional bioactive components were also measured by commercially available assays: ghrelin, insulin, leptin, adiponectin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and glucose. Bioactive components in normal weight and obese mothers were compared using unpaired t-test (parametric) and Mann–Whitney U-test (non-parametric), as appropriate.ResultsThe primary findings of this study are that the adipokine CTRP3 is present in BM and CTRP3 levels are increased with pregravid obesity. Additionally, this study independently confirmed previous work that BM from obese mothers has a higher concentration of insulin and leptin. Further, no differences were observed in BM between obese and normal weight mothers in ghrelin, adiponectin, IL-6, TNF-α, or glucose levels.ConclusionThis study identified a novel factor in BM, CTRP3, and showed that BM CTRP3 levels higher in obese mothers. Because of the purported insulin sensitizing effect of CTRP3, it is possible that the elevated levels of CTRP3 in the BM of obese mothers may offset negative effects of elevated leptin and insulin levels in the BM of obese mothers. Future studies will need to be conducted to determine the relevance of CTRP3 in BM and to examine the presence of other adipose tissue-derived hormonal factors.

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“…Adipose tissue is a major contributor to whole body insulin sensitivity 40 and this tissue is particularly vulnerable to the effects of developmental programming 12 , 41 , 42 . Although para-ovarian fat pad mass was increased in F2 recuperated animals, no effect of grand-maternal diet upon adipocyte cell size was observed.…”

Section: Discussionmentioning

confidence: 99%

Insulin-signalling dysregulation and inflammation is programmed trans-generationally in a female rat model of poor maternal nutrition

Tarry-Adkins

Aiken

Ashmore

et al. 2018

Sci Rep

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Developmental programming phenotypes can be recapitulated in subsequent generations not directly exposed to the initial suboptimal intrauterine environment. A maternal low-protein diet during pregnancy and postnatal catch-up growth (‘recuperated’) alters insulin signaling and inflammation in rat offspring (F1-generation). We aimed to establish if this phenotype is also present in F2-generation females. Insulin-receptor-substrate-1 protein expression was decreased in para-ovarian adipose tissue at 3 months in offspring exposed to a grand-maternal low-protein diet (F2-recuperated), vs. F2-control animals (p < 0.05). There was no effect of grand-maternal diet upon Insulin-receptor-substrate-1 mRNA. Protein-kinase C-zeta protein levels were increased at 3 and 6 months in F2-recuperated animals (p < 0.01 at both ages). Phosphorylated-Aktser473 levels were decreased in F2-recuperated animals (p < 0.001). Interleukin-1β protein levels were increased at 3 (p < 0.01) and (p < 0.001) 6 months in F2-recuperated animals. Vastus-lateralis insulin-receptor-β protein expression (p < 0.001) and pAktser473 (p < 0.01) were increased at 3 months in F2-recuperated animals compared to controls. At 6 months, PAktser473 was lower in F2-recuperated animals (p < 0.001). Aspects of insulin signalling dysregulation and inflammation present in offspring of low-protein fed dams can be transmitted to subsequent generations without further exposure to a suboptimal maternal diet. These findings contribute to our understanding of insulin-resistance in grandchildren of sub-optimally nourished individuals during pregnancy.

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Rats perinatally exposed to food restriction and high-fat diet show differences in adipose tissue gene expression under chronic caloric restriction

Cited by 10 publications

References 50 publications

Coenzyme Q10 Prevents Insulin Signaling Dysregulation and Inflammation Prior to Development of Insulin Resistance in Male Offspring of a Rat Model of Poor Maternal Nutrition and Accelerated Postnatal Growth

Coenzyme Q10 Prevents Insulin Signaling Dysregulation and Inflammation Prior to Development of Insulin Resistance in Male Offspring of a Rat Model of Poor Maternal Nutrition and Accelerated Postnatal Growth

The adipokine C1q TNF related protein 3 (CTRP3) is elevated in the breast milk of obese mothers

Insulin-signalling dysregulation and inflammation is programmed trans-generationally in a female rat model of poor maternal nutrition

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