Dietary zinc deficiency impairs desaturation and elongation of linoleic acid, but nothing is so far known about its effects on net whole-body utilization of linoleic or alpha-linolenic acids. By measuring intake, whole-body accumulation, and excretion of linoleic and alpha-linolenic acids, together with accumulation of their long-chain products, we hypothesized that a quantitative estimate could be obtained of their whole-body disappearance (apparent oxidation). This was evaluated in pregnant and non-pregnant rats given a low-zinc diet (3.4 vs. 34 mg zinc/kg diet in zinc-adequate controls). In the nonpregnant controls, low zinc intake did not significantly affect food intake or weight gain but did reduce whole-body accumulation of desaturated and (or) elongated products of linoleic and alpha-linolenic acids. In pregnant rats, low zinc intake reduced food intake and weight gain and doubled whole-body disappearance of linoleic and alpha-linolenic acids relative to that in the zinc-adequate controls. In contrast to the maternal fatty acid changes, low zinc intake had no significant effect on linoleic acid accumulation in the fetuses. We conclude that low zinc intake during pregnancy prevents the normal accumulation of long-chain fatty acids and differentially depletes maternal whole-body stores of linoleic and alpha-linolenic acids.
Subclinical hypothyroidism (SCH) has been shown to be associated with microbiota. However, the association between SCH and oral microbiota has not yet been elucidated. The results of our previous clinical studies showed that Prevotella intermedia was abundant in the oral microbiota of SCH patients. This study aimed to investigate the relationship between SCH and oral microbiota, verify the pathogenicity of P. intermedia in SCH, and preliminarily explore the possible mechanism. The SCH mouse model with oral application of P. intermedia was established, and the variance in the mouse oral microbiota and changes in thyroid function and metabolism were detected in mice. Student’s t test and analysis of variance were used for statistical analysis. Oral application of P. intermedia changed the composition of the oral microbiota of SCH mice, which enhanced the damage to the thyroid and decreased the expression of functional genes of the thyroid. Moreover, P. intermedia decreased oxygen consumption and aggravated glucose and lipid metabolism disorders in SCH mice. Glucose tolerance and insulin tolerance decreased, and the triglyceride content of the liver and inflammatory infiltration in adipose tissue increased in SCH mice after P. intermedia stimulation. Mechanistically, P. intermedia increased the proportion of CD4+ T cells in cervical lymph nodes and thyroids in SCH mice. Th1 cells were suggested to play an important role in the pathogenesis of SCH involving P. intermedia. In conclusion, P. intermedia aggravated SCH manifestations, including thyroid dysfunction and glucose and lipid metabolism disorders, by causing immune imbalance in mice. This study sheds new light on the pathogenesis of SCH from the perspective of oral microbiota.
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