Iron plays a role in energy metabolism as a component of vital enzymes and electron transport chains (ETCs) for adenosine triphosphate (ATP) synthesis. The tricarboxylic acid (TCA) cycle and oxidative phosphorylation are crucial in generating ATP in mitochondria. At the mitochondria matrix, heme and iron-sulfur clusters are synthesized. Iron-sulfur cluster is a part of the aconitase in the TCA cycle and a functional or structural component of electron transfer proteins. Heme is the prosthetic group for cytochrome c, a principal component of the respiratory ETC. Regarding fat metabolism, iron regulates mitochondrial fat oxidation and affects the thermogenesis of brown adipose tissue (BAT). Thermogenesis is a process that increases energy expenditure, and BAT is a tissue that generates heat via mitochondrial fuel oxidation. Iron deficiency may impair mitochondrial fuel oxidation by inhibiting iron-containing molecules, leading to decreased energy expenditure. Although it is expected that impaired mitochondrial fuel oxidation may be restored by iron supplementation, its underlying mechanisms have not been clearly identified. Therefore, this review summarizes the current evidence on how iron regulates energy metabolism considering the TCA cycle, oxidative phosphorylation, and thermogenesis. Additionally, we relate iron-mediated metabolic regulation to obesity and obesity-related complications.
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Schizophrenia is a mental illness characterized by symptoms such as hallucinations, delusions, disorganized speech, disorganized or catatonic behavior, and negative symptoms (emotional flatness, apathy, and lack of speech). It causes social and economic burdens to patients and their family. Although etiology of schizophrenia is still uncertain, dopamine dysregulation is traditionally considered as a main etiological factor of schizophrenia, which has been utilized to develop drugs for treating schizophrenia. Recently, inflammation has presented being a risk factor for schizophrenia in that neuroinflammation contributes to the pathophysiology of schizophrenia and the exacerbation of symptom severity. Various factors including diet can regulate inflammatory state. Specific foods or dietary patterns have anti- or pro-inflammatory potentials. Increased levels of pro-inflammatory cytokines and microglia activation have been reported in schizophrenia populations and were related to the pathogenesis of schizophrenia. Omega-3 fatty acids were often recommended to schizophrenia patients because of their anti-inflammatory activities. In this review, we investigate the inflammation-related pathogenesis of schizophrenia and summarize potential nutritional approaches to inhibit the manifestation of symptoms and to alleviate symptom severity using anti-inflammatory nutrients or functional components.
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Blood glucose homeostasis is well maintained by coordinated control of various hormones including insulin and glucagon as well as cytokines under normal conditions. However, chronic exposure to diabetic environment with high fat/high sugar diets and physical/mental stress can cause hyperglycemia, one of main characteristics of insulin resistance, metabolic syndrome, and diabetes. Hyperglycemia impairs organogenesis and induces organ abnormalities such as cardiac defect
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The purpose of this study is to investigate whether nicotinic acid (NA) and nicotinamide (NAM) reduce the Alzheimer disease (AD)-related gene expression in brain tissues of amyloid beta (Aβ)-injected mice. Male Crj:CD1 (ICR) mice were divided into 6 treatment groups; 1) control, 2) Aβ control, 3) Aβ + NA 20 mg/kg/day (NA20), 4) Aβ + NA40, 5) Aβ + NAM 200 mg/kg/day (NAM200), and 6) Aβ + NAM400. After 1-week acclimation period, the mice orally received NA or NAM once a day for a total of 7 successive days. On day 7, biotinylated Aβ42 was injected into mouse tail vein. At 5 hours after the injection, blood and tissues were collected. Aβ42 injection was confirmed by Western blot analysis of Aβ42 protein in brain tissue. NAM400 pre-treatment significantly reduced the gene expression of amyloid precursor protein and presenilin 1 in brain tissues. And, NAM200 and NAM400 pre-treatments significantly increased sirtuin 1 expression in brain tissues, which is accompanied by the decreased brain expression of nuclear factor kappa B by 2 doses of NAM. Increased expression of AD-related genes was attenuated by the NAM treatment, which suggests that NAM supplementation may be a potential preventive strategy against AD-related deleterious changes.
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Sirtuin (SIRT) is a main regulator of metabolism and lifespan, and its importance has been implicated in the prevention against aging-related diseases. The purpose of this study was to identify the pattern of serum SIRT1 activity according to age and sex, and to investigate how serum SIRT1 activity is correlated with other metabolic parameters in Korean adults. The Biobank of Jeju National University Hospital, a member of the Korea Biobank Network, provided serum samples from 250 healthy adults. Aging- and metabolism-related factors were analyzed in serum, and the data were compared by the stratification of age and sex. Basal metabolic rate (BMR) decreased with age and was significantly lower in men in their fifties and older and in women in their forties and older compared with twenties in men and women, respectively. SIRT1 activities were altered by age and sex. Especially, women in their thirties showed the highest SIRT1 activities. Correlation analysis displayed that SIRT1 activity is positively correlated with serum triglyceride (TG) in men, and with waist circumference, systolic blood pressure, diastolic blood pressure, and serum TG in women. And, SIRT1 activity was negatively correlated with aspartate aminotransferase/alanine aminotransferase ratio in women (r = −0.183, p = 0.039). Positive correlation was observed between SIRT1 activity and BMR in women (r = 0.222, p = 0.027), but not in men. Taken together, these findings suggest the possibility that serum SIRT1 activities may be utilized as a biomarker of aging. In addition, positive correlation between SIRT1 activity and BMR in women suggests that serum SIRT1 activity may reflect energy expenditure well in human.
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Dietary intake and nutritional status of individuals are important factors affecting mental health and the development of psychiatric disorders. Majority of scientific evidence relating to mental health focuses on depression, cognitive function, and dementia, and limited evidence is available about other psychiatric disorders including schizophrenia. As life span of human being is increasing, the more the prevalence of mental disorders is, the more attention rises. Lists of suggested nutritional components that may be beneficial for mental health are omega-3 fatty acids, phospholipids, cholesterol, niacin, folate, vitamin B6, and vitamin B12. Saturated fat and simple sugar are considered detrimental to cognitive function. Evidence on the effect of cholesterol is conflicting; however, in general, blood cholesterol levels are negatively associated with the risk of depression. Collectively, the aims of this review are to introduce known nutritional factors for mental health, and to discuss recent issues of the nutritional impact on cognitive function and healthy brain aging.
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