The impact of diet upon mitochondrial physiology (Review)

Kyriazis, Ioannis D.; Vassi, Eleni; Alvanou, Maria; Angelakis, Christos; Tekos, Fotios; Garikipati, Venkata Naga Srikanth; Spandidos, Demetrios A.; Kouretas, Demetrios

doi:10.3892/ijmm.2022.5191

Cited by 28 publications

(16 citation statements)

References 204 publications

(283 reference statements)

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“…Brown adipose tissue (BAT) is another type of adipose tissue that consists of brown adipocytes, which participate in heat production for regulating body temperature [ 11 ]. One of the most characteristic features of brown adipocytes is that they possess enriched and metabolically active mitochondria [ 12 ]. Mitochondria are essential intracellular organelles that convert chemical energy derived from glucose and fatty acids into adenosine triphosphate (ATP) through the tricarboxylic acid (TCA) cycle, fatty acid β-oxidation, and electron transport chain (ETC).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Energy Metabolism in the Regulation of Thermogenic Brown Fats and Human Metabolic Diseases

Takeda

Harada

Yoshikawa

et al. 2023

IJMS

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Brown fats specialize in thermogenesis by increasing the utilization of circulating blood glucose and fatty acids. Emerging evidence suggests that brown adipose tissue (BAT) prevents the incidence of obesity-associated metabolic diseases and several types of cancers in humans. Mitochondrial energy metabolism in brown/beige adipocytes regulates both uncoupling protein 1 (UCP1)-dependent and -independent thermogenesis for cold adaptation and the utilization of excess nutrients and energy. Many studies on the quantification of human BAT indicate that mass and activity are inversely correlated with the body mass index (BMI) and visceral adiposity. Repression is caused by obesity-associated positive and negative factors that control adipocyte browning, de novo adipogenesis, mitochondrial energy metabolism, UCP1 expression and activity, and noradrenergic response. Systemic and local factors whose levels vary between lean and obese conditions include growth factors, inflammatory cytokines, neurotransmitters, and metal ions such as selenium and iron. Modulation of obesity-associated repression in human brown fats is a promising strategy to counteract obesity and related metabolic diseases through the activation of thermogenic capacity. In this review, we highlight recent advances in mitochondrial metabolism, thermogenic regulation of brown fats, and human metabolic diseases.

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Section: Introductionmentioning

confidence: 99%

Mitochondrial Energy Metabolism in the Regulation of Thermogenic Brown Fats and Human Metabolic Diseases

Takeda

Harada

Yoshikawa

et al. 2023

IJMS

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“…As underlined by many authors, KD can promote mitochondrial health by improving mitochondrial activity, stimulating the genesis of new mitochondria and remodeling [15,45,[57][58][59][60][61].…”

Section: Kd and Mitochondriamentioning

confidence: 97%

“…Mitochondria are dynamic structures and their number and function are regulated by the interaction between internal factors and external variables through complex mecha-nisms. Among external variables, food and physical exercise are the most important factors able to influence mitochondria physiology [57].…”

Section: Kd and Mitochondriamentioning

confidence: 99%

Investigating the Link between Ketogenic Diet, NAFLD, Mitochondria, and Oxidative Stress: A Narrative Review

Paoli

Cerullo

2023

Antioxidants

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Together with the global rise in obesity and metabolic syndrome, the prevalence of individuals who suffer from nonalcoholic fatty liver disease (NAFLD) has risen dramatically. NAFLD is currently the most common chronic liver disease and includes a continuum of liver disorders from initial fat accumulation to nonalcoholic steatohepatitis (NASH), considered the more severe forms, which can evolve in, cirrhosis, and hepatocellular carcinoma. Common features of NAFLD includes altered lipid metabolism mainly linked to mitochondrial dysfunction, which, as a vicious cycle, aggravates oxidative stress and promotes inflammation and, as a consequence, the progressive death of hepatocytes and the severe form of NAFLD. A ketogenic diet (KD), i.e., a diet very low in carbohydrates (<30 g/die) that induces “physiological ketosis”, has been demonstrated to alleviate oxidative stress and restore mitochondrial function. Based on this, the aim of the present review is to analyze the body of evidence regarding the potential therapeutic role of KD in NAFLD, focusing on the interplay between mitochondria and the liver, the effects of ketosis on oxidative stress pathways, and the impact of KD on liver and mitochondrial function.

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“…Adapted from (226) The topic of mitochondrial adaptation to nutrient availability was addressed by Liesa and Shirihai in 2013 (227). In 2022 Kyriazis et al, described processes of mitochondrial adaptation to changes in diet (Figure 5 in (228)). The simplistic idea that dietary evaluations and simple calory counting reflect the level of energetics in the body contradict this physiological principle.…”

Section: I) Sepsis and Critical Illnessmentioning

confidence: 99%

From the Thyroid to the Heart

Moncayo¹,

Moncayo²

2023

GJMR

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The pathogenesis of human disease is commonly considered to be unique to each organ or system. This has led to specialization in medical practice leaving little space for global pathogenesis concepts. In this review we have departed from a biochemical concept of coenzyme Q10 (CoQ10) deficiency and its relation to the initiation of hypoxia response in a systemic way. Several conditions of secondary CoQ10 deficiency are known in the literature by which the organs involved could be affected by hypoxia and switch to glycolytic metabolism. The most salient biomarkers of this situation are the low T3 syndrome and the elevation of IL-6. These parameters together with CoQ10 deficiency delineate a condition of acquired mitochondrial dysfunction. Additional related biochemical deficiency conditions affect magnesium, selenium, and iron levels. Visualization of glycolysis can be clearly achieved by diagnostic imaging methods based on the use of 18F-fluoro-deoxyglucose (18F-FDG). We present several examples of diagnostic imaging with 18F-FDG to demonstrate our model of acquired mitochondrial dysfunction and disease.

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The impact of diet upon mitochondrial physiology (Review)

Cited by 28 publications

References 204 publications

Mitochondrial Energy Metabolism in the Regulation of Thermogenic Brown Fats and Human Metabolic Diseases

Mitochondrial Energy Metabolism in the Regulation of Thermogenic Brown Fats and Human Metabolic Diseases

Investigating the Link between Ketogenic Diet, NAFLD, Mitochondria, and Oxidative Stress: A Narrative Review

From the Thyroid to the Heart

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