High oleic/stearic fatty-acid desaturation index in cord plasma from infants of mothers with gestational diabetes

Yee, Jennifer K.; Mao, Catherine S.; Ross, Michael G.; Lee, W N P; Desai, Mina; Toda, Ayumi; Kjos, Siri L.; Hicks, Rebecca; Patterson, Mary E.

doi:10.1038/jp.2014.23

Cited by 16 publications

(16 citation statements)

References 45 publications

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“…Total free fatty acids, as well as individual lipids including palmitate (16:0), stearate (18:0), and triglycerides containing 18:3w6, 22:4w6, 22:5w6 and 20:4, were significantly increased in cord blood from infants of ov-ob women. Moreover, the ratio of 18:1n9 to 18:0, a surrogate for SCD1 delta-9 desaturase activity, was increased in the ov-ob group, similar to patterns in infants of women with gestational diabetes (47). By contrast, lipid species containing 20:3w6 fatty acids (e.g.…”

Section: Discussionsupporting

confidence: 57%

Maternal obesity programs mitochondrial and lipid metabolism gene expression in infant umbilical vein endothelial cells

et al. 2016

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Background/Objectives Maternal obesity increases risk for childhood obesity, but molecular mechanisms are not well understood. We hypothesized that primary umbilical vein endothelial cells (HUVEC) from infants of overweight and obese mothers would harbor transcriptional patterns reflecting offspring obesity risk. Subjects/Methods In this observational cohort study, we recruited 13 lean (pre-pregnancy BMI <25.0 kg/m2) and 24 overweight-obese (‘ov-ob’, BMI ≥25.0 kg/m2) women. We isolated primary HUVEC, and analyzed both gene expression (Primeview, Affymetrix) and cord blood levels of hormones and adipokines. Results 142 transcripts were differentially expressed in HUVEC from infants of overweight-obese mothers (false discovery rate, FDR <0.05). Pathway analysis revealed that genes involved in mitochondrial and lipid metabolism were negatively correlated with maternal BMI (FDR <0.05). To test whether these transcriptomic patterns were associated with distinct nutrient exposures in the setting of maternal obesity, we analyzed the cord blood lipidome and noted significant increases in levels of total free fatty acids (lean: 95.5 ± 37.1 ug/ml, ov-ob: 124.1 ± 46.0 ug/ml, P=0.049), palmitate (lean: 34.5 ± 12.7 ug/ml, ov-ob: 46.3 ± 18.4 ug/ml, P=0.03) and stearate (lean: 20.8 ± 8.2 ug/ml, ov-ob: 29.7 ± 17.2 ug/ml, P=0.04), in infants of overweight-obese mothers. Conclusion Prenatal exposure to maternal obesity alters HUVEC expression of genes involved in mitochondrial and lipid metabolism, potentially reflecting developmentally-programmed differences in oxidative and lipid metabolism.

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Section: Discussionsupporting

confidence: 57%

Maternal obesity programs mitochondrial and lipid metabolism gene expression in infant umbilical vein endothelial cells

et al. 2016

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“…However, few mechanistic studies have addressed the role of altered fatty acid metabolism in the underlying mechanism of programmed obesity. In adults, fatty acid DI and SCD-1 activity have been shown to positively correlate with lipogenesis and adiposity [16, 21, 31, 32]. In the current study, despite being weaned to the control diet and having a suppressed C16 desaturase pathway at birth, the HF male offspring developed increased plasma and liver DI, increased liver SCD-1 expression, and obesity as adults.…”

Section: Discussionmentioning

confidence: 58%

“…Although we did not measure liver TAG in our study, other studies of maternal high-fat diets have shown increased liver TAGs in the offspring as early as ages day 1 and day 10 [34, 35]. Hence, increased de novo production fatty acids and their storage as TAG may contribute to the development of obesity in this model of programming by maternal HF diet [16, 21, 31, 32]. Dietary fat content and composition affect the composition of lipids secreted in rats’ milk [36–38], which may contribute to the programmed offspring phenotype [10, 11].…”

Section: Discussionmentioning

confidence: 89%

“…The extraction of total fatty acids (including those from phospholipids, TAG, cholesterol esters, and free fatty acids) from plasma and liver tissue was performed, as previously described [21]. Tissue samples (~15 mg liver) or plasma samples (30 µl) were saponified overnight in equal volumes (100 µl) of 200-proof ethanol and 30 % KOH (w/v) on a 70 °C heating block.…”

Section: Methodsmentioning

confidence: 99%

“…Hence, the DI of palmitoleic/palmitic and (vaccenic + palmitoleic)/palmitic represent activity of the 16-carbon (C16) desaturation pathway, whereas oleic/stearic represents activity of the 18-carbon (C18) desaturation pathway. Notably, both the DI and SCD-1 activity correlate with measures of adiposity [18–21]. …”

Section: Introductionmentioning

confidence: 99%

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Maternal High‐Fat‐Diet Programs Rat Offspring Liver Fatty Acid Metabolism

Seet

Yee

Jellyman

et al. 2015

Lipids

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In offspring exposed in utero to a maternal diet high in fat (HF), we have previously demonstrated that despite similar birth weights, HF adult offspring at 6 months of age had significantly higher body weights, greater adiposity, and increased triacylglycerol (TAG) levels as compared to controls. We hypothesized that a maternal HF diet predisposes to offspring adiposity via a programmed increase in the synthesis of monounsaturated fatty acids in the liver and hence increased substrate availability for liver TAG synthesis. We further hypothesized that programmed changes in offspring liver fatty acid metabolism are associated with increased liver expression of the lipogenic enzyme stearoyl-CoA desaturase-1 (SCD-1). Female rats were maintained on a HF diet rich in monounsaturated fatty acids (MUFA) prior to and throughout pregnancy and lactation. After birth, newborns were nursed by the same dam, and all offspring were weaned to control diet. Plasma and liver fatty acid compositions were determined using gas chromatography/mass spectrometry. Fatty acid C16 desaturation indices of palmitoleic/palmitic and (vaccenic + palmitoleic)/palmitic and the C18 desaturation index of oleic/stearic were calculated. Liver protein abundance of SCD-1 was analyzed in newborns and adult offspring. Plasma and liver C16 desaturation indices were decreased in HF newborns, but increased in the adult offspring. Liver SCD-1 expression was increased in the HF adult offspring. These data show that the maternal HF diet during pregnancy and lactation increases offspring liver SCD-1 protein abundance and alters the liver C16 desaturase pathway.

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Nuclear magnetic resonance spectroscopy reveals dysregulation of monounsaturated fatty acid metabolism upon SPINK1 attenuation in colorectal cancer

et al. 2022

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Metabolic reprogramming, a key hallmark of cancer, plays a pivotal role in fulfilling the accelerated biological demands of tumor cells. Such metabolic changes trigger the production of several proinflammatory factors, thereby inciting cancer development and its progression. Serine protease inhibitor Kazal Type 1 (SPINK1), well known for its oncogenic role and its upregulation via acute-phase reactions, is highly expressed in multiple cancers including colorectal cancer (CRC). Here, we show accumulation of lipid droplets in CRC cells stained with Oil Red O upon SPINK1 silencing.Furthermore, NMR spectroscopy analysis revealed an accretion of monounsaturated fatty acids (MUFAs) and phosphatidylcholine in these CRC cells, while the levels of polyunsaturated fatty acids remained unaltered. This alteration indicates the presence of MUFAs with the triglycerides in the lipid droplets as observed in SPINK1silenced CRC cells. Considering the role of MUFAs in the anti-inflammatory response, our data hint that suppression of SPINK1 in CRC leads to activation of an antiinflammatory signaling milieu. Conclusively, our study uncovers a connection between lipid metabolism and SPINK1-mediated CRC progression, hence paving the way for further exploration and better prognosis of SPINK1-positive CRC patients.

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High oleic/stearic fatty-acid desaturation index in cord plasma from infants of mothers with gestational diabetes

Cited by 16 publications

References 45 publications

Maternal obesity programs mitochondrial and lipid metabolism gene expression in infant umbilical vein endothelial cells

Maternal obesity programs mitochondrial and lipid metabolism gene expression in infant umbilical vein endothelial cells

Maternal High‐Fat‐Diet Programs Rat Offspring Liver Fatty Acid Metabolism

Nuclear magnetic resonance spectroscopy reveals dysregulation of monounsaturated fatty acid metabolism upon SPINK1 attenuation in colorectal cancer

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