Association between polyunsaturated fatty acid intake and infertility among American women aged 20-44 years.

Background: Infertility is a nationwide public health priority in the U.S. However, few studies have investigated the effects of dietary intake of polyunsaturated fatty acids (PUFAs) on female infertility. This study explored the association between PUFA intake and risk of infertility. Methods: A total of 1,785 women aged 20-44 years from three National Health and Nutrition Examination Survey cycles (2013-2018) were included in this cross-sectional study. The intake of PUFAs was obtained from a 24-h dietary interview on two separate days with a 3-10-day interval, and nutrient residue models were used. Fertility status was assessed by positive response to two relative questions via a questionnaire. Logistic regression models were used and some covariates were adjusted. Results: Among all the participants, 340 (19.05%) women suffered from infertility. The intake of docosahexaenoic acid (DHA) (OR = 0.998, 95% CI 0.998, 0.009) was slightly related to the risk of infertility. In contrast, women with higher α-linolenic acid (ALA) (OR = 1.416, 95% CI 1.138, 1.763) and linoleic acid (LA) intake (OR = 1.020, 95% CI 1.002, 1.038) presented with a relatively higher risk of primary infertility. Furthermore, in 20-34-year-old women, higher omega-6/omega-3 was significant associated with the risk of infertility (OR = 1.002, 95%CI 1.000, 1.005). Conclusions: Our results suggest that PUFA intake is only slightly associated with infertility. The higher the DHA intake, the lower the risk of infertility regardless of age. In women with primary infertility, ALA and LA has negative effect.

Prenatal low-dose DEHP exposure induces metabolic adaptation and obesity: Role of hepatic thiamine metabolism.

Di-(2-ethylhexyl)-phthalate (DEHP) is a ubiquitous environmental pollutant and is widely used in industrial plastics. However, the long-term health implications of prenatal exposure to DEHP remains unclear. We set out to determine whether prenatal DEHP exposure can induce metabolic syndrome in offspring and investigate the underlying mechanisms. A mouse model of prenatal DEHP exposure (0.2, 2, and 20 mg/kg/day) was established to evaluate the long-term metabolic disturbance in offspring. The mice were profiled for the hepatic metabolome, transcriptome and gut microbiota to determine the underlying mechanisms. Thiamine supplementation (50 mg/kg/day) was administered to offspring to investigate the role of thiamine in ameliorating metabolic syndrome. Prenatal exposure to low-dose DEHP (0.2 mg/kg/day) resulted in metabolic syndrome, including abnormal adipogenesis, energy expenditure and glucose metabolism, along with dysbiosis of the gut microbiome, in male offspring. Notably, hepatic thiamine metabolism was disrupted in these offspring due to the dysregulation of thiamine transport enzymes, which caused abnormal glucose metabolism. Prenatal low-dose DEHP exposure caused life-long metabolic consequences in a sex-dependent manner, and these consequences were be attenuated by thiamine supplementation in offspring. Our findings suggest low-dose DEHP exposure during early life stages is a potential risk factor for later obesity and metabolic syndrome.

An NMR-Based Metabolomic Approach to Unravel the Preventive Effect of Water-Soluble Extract from Dendrobium officinale Kimura & Migo on Streptozotocin-Induced Diabetes in Mice.

Dendrobium officinale Kimura & Migo (D. officinale) is a precious herbal medicine. In this study, we investigated metabolic mechanism underlying the effect of D. officinale water extract (DOWE) on diabetes prevention in mice after streptozotocin (STZ) exposure using NMR-based metabolomics. Interestingly, we found a decrease in blood glucose and an increase in liver glycogen in mice pretreated with DOWE after STZ exposure. The DOWE pretreatment significantly increased citrate and glutamine in the serum as well as creatine, alanine, leucine, isoleucine, valine, glutamine, glutathione and taurine in the liver of STZ-treated mice. Furthermore, serum glucose was significantly negatively correlated with citrate, pyruvate, alanine, isoleucine, histidine and glutamine in the serum as well as alanine and taurine in the liver. These findings suggest that the effect of DOWE on diabetes prevention may be linked to increases in liver glycogen and taurine as well as the up-regulation of energy and amino acid metabolism.