Annual review of nutrition最新文献

Diet quality has been proposed as a determinant of brain aging, which has attracted considerable attention given the current global demographic shift toward older age. Comprehensive global systematic reviews that have explored dietary patterns and brain aging highlight a recurrent theme. Any healthy dietary pattern that includes higher consumption of vegetables, fruits, legumes, nuts, fish and/or seafood, and unsaturated vegetable oils/fats and lower consumption of red and processed meats and sugar-sweetened beverages is associated with lower risk of age-related neurodegenerative disease. The biologic mechanism(s) underlying these cognitive protective effects are unknown. Furthermore, it is unlikely that consumption of a healthy dietary pattern alone will achieve clinically relevant success in reducing risk of cognitive decline and/or dementia given that there is no single risk factor that accounts for the variation in brain aging.

There is widespread interest in fasting as a therapeutic or preventive regimen for improving health. This review provides an overview of the impact of fasting on adipose tissue metabolism, with special attention to sexually dimorphic regulation. During fasting, the storage of triacylglycerols in adipose tissue is inhibited via suppression of the extracellular lipolytic enzyme lipoprotein lipase. By contrast, the breakdown of stored triacylglycerols and subsequent release of fatty acids and glycerol in the blood are enhanced via stimulation of the intracellular lipolytic enzymes adipose triglyceride lipase and hormone-sensitive lipase. These metabolic alterations are driven by changes in humoral factors such as insulin, glucagon, corticosteroids, growth hormone, and catecholamines, as well as by neuronal pathways, and are mediated by transcriptional and posttranscriptional regulation of critical enzymes. Overall, fasting profoundly influences adipose tissue metabolism and leads to mobilization of stored triacylglycerols and the repartitioning of circulating triacylglycerols to nonadipose tissues.

Folate and vitamin B₁₂ (B12) are essential cofactors in folate-mediated one-carbon metabolism (FOCM). FOCM includes a series of methyl transfer reactions for methionine regeneration and de novo synthesis of nucleotides, including thymidylate. Deficiency in either folate or B12 can result in negative health outcomes including megaloblastic anemia, with additional neurocognitive impairments observed as a result of B12 deficiency. While folate deficiency is not common in the United States due to mandatory folic acid fortification, B12 deficiency is observed more frequently, particularly in certain subpopulations such as vegetarians/vegans and older adults. Fortification of the food supply with folic acid has been effective to increase folate status and reduce the incidence of birth defects. However, consumption of fortified foods and use of dietary supplements containing folic acid have led to an increase in the proportion of individuals exceeding the tolerable upper intake level of folic acid. Although the interaction between folate and B12 has been appreciated for decades in relation to megaloblastic anemia, it has been recently proposed that elevated serum folate may worsen neurocognitive effects and other metabolic impairments (altered glucose homeostasis, type 2 diabetes in offspring) associated with B12 deficiency. This review highlights molecular mechanisms that may explain the biology underlying these associations with a focus on findings from studies in model systems.

My scientific journey is not traditional; it begins with the career opportunities available for and expectations of young women during the outset of the women's liberation era and how life changed along the way. I've started my story when I was a child in the 1950s, daughter of a milkman and an immigrant fleeing the communists in her home country. My story reaches an apex when I became an internationally recognized vitamin E expert. Overall, I made transformative contributions to our understanding of α-tocopherol function in humans, and, using model systems, I have reported how its absence has a major impact on cellular metabolism. This is the story of my transformation. I have had some excellent mentors. I have a passion about learning why the body needs α-tocopherol. Certainly, when I started out, I had no expectations that I would become a world-renowned scientist, a term I now use to describe myself.

Dietary bioactive compounds such as omega-3 polyunsaturated fatty acids and phytochemicals have numerous health benefits, which include alleviating obesity-associated inflammation and metabolic dysfunction. While mechanistic studies have focused thus far on how these compounds or their metabolites affect whole-animal physiology or exert tissue-specific effects, detailed reports are lacking about how these bioactives specifically affect gut microbiota and mitochondrial function, two important processes impacted by metabolic diseases. Gut microbiota, through their composition and metabolites, play a significant role in overall health and mediating the effects of diet. Therefore, understanding how dietary bioactive compounds modulate gut microbiota is crucial for elucidating their contributions to metabolic health. Conversely, gut microbiota may also alter the metabolism of bioactives, especially phytochemicals, and impact their bioavailability and function. Mitochondria, particularly in adipose tissue, play a central role in energy metabolism and are implicated in the development of obesity-associated metabolic dysfunction. Thus, investigating the effects of dietary bioactive compounds on mitochondrial function provides valuable insight into their potential roles in addressing obesity-related diseases. Accordingly, the goal of this review is to discuss key published work on the interplay between dietary bioactives, gut microbiota and their metabolites, and mitochondria function in the context of improving obesity-associated inflammation and metabolic dysfunction.

Dietary guidelines have been placed under unprecedented scrutiny in the past decade, as the "obesity epidemic" enters its fifth decade with limited evidence of public health progress. In the era of successful obesity pharmacotherapy, there is a heightened sense of urgency to make progress on dietary prevention of obesity and related chronic diseases, contributing to both diverse criticism of guidelines and low degrees of trust in nutritional sciences. In this review, I view nutritional guidance through a historical lens, tracking its development from its genesis through the modern focus on obesity and chronic diseases and consider criticisms of past and existing dietary guidance. I reflect on themes that emerge from this history and consider potential paths forward to improve the quality of nutritional guidance and actualize its goals of improving population health.

Hexoses, including glucose, fructose, and galactose, are six-carbon monosaccharides that play fundamental roles in mammalian metabolism, with glucose serving as the primary energy source and fructose and galactose metabolized through pathways converging with glucose metabolism. While glucose metabolism has been extensively studied over the past hundred years, the mechanisms of fructose metabolism and uptake, the transporters involved, and its roles in physiology and disease are far less explored. Recent data also suggest that excessive fructose intake can have detrimental effects on metabolic organs, including the liver. Emerging studies have uncovered novel regulatory mechanisms in glucose and fructose metabolism, including the role of posttranslational modifications of transporters and enzymes, and the discovery of regulators of transporters. Here, we highlight new findings on the regulation of glucose and fructose transporters and integrate recent molecular and clinical insights into how glucose and fructose contribute to metabolic diseases.

The time of day that we eat is increasingly recognized as contributing as importantly to overall health as the amount or quality of the food we eat. The endogenous circadian clock has evolved to promote intake at optimal times when an organism is intended to be awake and active, but electric lights and abundant food allow eating around the clock with deleterious health outcomes. In this review, we highlight literature pertaining to the effects of food timing on health, beginning with animal models and then translation into human experiments. We emphasize the pitfalls and opportunities that technological advances bring in bettering understanding of eating behaviors and their association with health and disease. There is great promise for restricting the timing of food intake both in clinical interventions and in public health campaigns for improving health via nonpharmacological therapies.

The global prevalence of type 2 diabetes mellitus (T2D) is increasing rapidly, with an anticipated 600 million cases by 2035. While infectious diseases such as helminth infections have decreased due to improved sanitation and health care, recent research suggests a link between helminth infections and T2D, with helminths such as Schistosoma, Nippostrongylus, Strongyloides, and Heligmosomoides potentially mitigating or slowing down T2D progression in human and animal models. Helminth infections enhance host immunity by promoting interactions between innate and adaptive immune systems. In T2D, type 1 immune responses are suppressed and type 2 responses are augmented, expanding regulatory T cells and innate immune cells, particularly type 2 immune cells and macrophages. This article reviews recent research shedding light on the favorable effects of helminth infections on T2D. The potential defense mechanisms identified include heightened insulin sensitivity and reduced inflammation. The synthesis of findings from studies investigating parasitic helminths and their derivatives underscores promising avenues for defense against T2D.

The dietary choices a mother makes during pregnancy offer her developing fetus its earliest exposure to the family's culinary preferences. This comprehensive literature review synthesizes five decades of research, which has provided valuable insights into fetal flavor learning. Converging evidence across various species supports the functionality of fetal chemoreceptive systems by the end of gestation, enabling the detection of an extensive array of chemosensory cues derived from the maternal diet and transmitted to the amniotic fluid. The fetus effectively encodes these flavors, resulting in their enhanced acceptance after birth. While existing studies predominantly concentrate on fetal learning about odor volatiles, limited evidence suggests a capacity for learning about gustatory (i.e., taste) properties. Examining whether these prenatal odor, taste, and flavor experiences translate into enduring shifts in dietary behaviors beyond weaning remains a crucial avenue for further investigation.