Feast and famine: Adipose tissue adaptations for healthy aging

Barbato, Daniele Lettieri; Aquilano, Katia

doi:10.1016/j.arr.2016.05.007

Cited by 36 publications

(20 citation statements)

References 98 publications

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“…Deterioration of sAT inevitably results in metabolic complications and accelerates aging. Actually, sAT represents the main storage and buffering system against excess of nutrients, avoiding visceral and ectopic fat accumulation [ 6 ]. Adipose tissue expansion can occur through an enlargement in adipocyte size or an increase in adipocyte number.…”

Section: Discussionmentioning

confidence: 99%

“…There is common consensus that enlargement of vAT increases the risk of developing age-related metabolic dysfunctions including type 2 diabetes and is more strongly correlated to such disease states than sAT. On the contrary, retention of a high ratio of functioning sAT to vAT is associated with increased health span and longevity [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

“…When nutrients are in excess, mitochondria may undergo indecision in the selection of the substrates thus failing in properly adjusting their metabolic activity [ 8 ]. Furthermore, a massive mitochondrial electron transport chain activity and oxidative damage could be operative thus leading to the exhaustion of the metabolic capacity of cells such as adipocytes [ 6 ]. Recently, it has been demonstrated that the decrease of NAD + , occurring during aging or upon nutrient excess is the triggering factor of mitochondrial dysfunction and acquirement of a senescent and secretory phenotype in many cells and tissues [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

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Maternal high calorie diet induces mitochondrial dysfunction and senescence phenotype in subcutaneous fat of newborn mice

et al. 2017

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Mitochondrial dysfunction, inflammation and senescence-like features are observed in adipose depots in aging and obesity. Herein, we evaluated how maternal high calorie diet (HCD) may impact on subcutaneous adipose tissue (sAT) of the newborn mice. Adult C57BL/6J mice were randomly divided in three groups: normal calorie diet (NCD), HCD and HCD supplemented with niacin 8 weeks before mating. Mothers and pups were then sacrificed and metabolic and molecular analyses were carried out on sAT. HCD induced mitochondria dysfunction in mothers without inflammation and senescence, whereas in pups we also revealed the occurrence of senescent phenotype. The mitochondrial dysfunction-associated senescence in pups was accompanied by a drop in NAD+/NADH ratio and alteration in the NAD+-dependent enzymes PARP1 and SIRT1. Importantly, maternal dietary supplementation with niacin during gestation and lactation restrained NAD+/NADH decrease imposed by HCD limiting inflammatory cytokine production and senescence phenotype in newborn sAT. Given the fundamental role of sAT in buffering nutrient overload and avoiding pathogenic ectopic fat accumulation, we suggest that NAD+ boosting strategies during maternal HCD could be helpful in limiting sAT dysfunction in newborn.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Maternal high calorie diet induces mitochondrial dysfunction and senescence phenotype in subcutaneous fat of newborn mice

et al. 2017

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“…Metabolic adaptation responses are essential to preserve energy homeostasis for basic functions in the organism during fasting. Fasting has a wide range of beneficial effects because it induces protective stress pathways that prevent and/or recover tissue damages; on the contrary, non-physiological, prolonged fasting could be involved in the cell death response governing numerous pathological processes [ 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 ]. Fasting has the potential to counter chronic metabolic disorders and improve health and lifespan; by contrast, misguided responses are potentially devastating and can also contribute to diverse types of muscular dysfunctions, like myotonic dystrophy type 1 [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Fasting Drives Nrf2-Related Antioxidant Response in Skeletal Muscle

Lettieri-Barbato

Minopoli

Caggiano

et al. 2020

IJMS

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A common metabolic condition for living organisms is starvation/fasting, a state that could play systemic-beneficial roles. Complex adaptive responses are activated during fasting to help the organism to maintain energy homeostasis and avoid nutrient stress. Metabolic rearrangements during fasting cause mild oxidative stress in skeletal muscle. The nuclear factor erythroid 2-related factor 2 (Nrf2) controls adaptive responses and remains the major regulator of quenching mechanisms underlying different types of stress. Here, we demonstrate a positive role of fasting as a protective mechanism against oxidative stress in skeletal muscle. In particular, by using in vivo and in vitro models of fasting, we found that typical Nrf2-dependent genes, including those controlling iron (e.g., Ho-1) and glutathione (GSH) metabolism (e.g., Gcl, Gsr) are induced along with increased levels of the glutathione peroxidase 4 (Gpx4), a GSH-dependent antioxidant enzyme. These events are associated with a significant reduction in malondialdehyde, a well-known by-product of lipid peroxidation. Our results suggest that fasting could be a valuable approach to boost the adaptive anti-oxidant responses in skeletal muscle.

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“…These conditions contribute to increased risk for metabolic perturbations such as insulin resistance, impaired glucose tolerance and diabetes [18,20]. Of importance, key processes of adipose tissue physiology affect molecular pathways that regulate lifespan [21], such as sirtuins (SIRTs) levels decline with age in several tissues, including adipose tissue, and this reduction induces adipocyte dysfunctions leading to obesity [6,22].…”

Section: Introductionmentioning

confidence: 99%

Browning of Adipose Tissue and Sirtuin Involvement

Favero¹,

Krajčíková²,

Bonomini³

et al. 2018

Adipose Tissue

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Obesity is an important risk factor for many diseases, including cardiovascular diseases, metabolic syndrome and cancers. Excessive dietary intake of caloric food results in its accumulation in white adipose tissue (WAT), whereas energy expenditure by fat utilization and oxidation predominately occurs in brown adipose tissue (BAT). Reducing obesity has become an important prevention strategy of research interest, focusing in the recent years, mainly on browning of WAT, the process during which the enhance of the mitochondria biogenesis occurs and then white adipocytes are converted to metabolically active beige adipocytes. Sirtuin1 (SIRT1), the most known isoform of sirtuin deacetylases, is implied in the browning of WAT process. In fact, it is a sensitive sensor of cell energy metabolism and, together with other sirtuin isoforms, contributes to this differentiation process. This chapter provides an overview about SIRT1 involvement in browning of WAT as a target molecule that can thereby contrast obesity.

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Feast and famine: Adipose tissue adaptations for healthy aging

Cited by 36 publications

References 98 publications

Maternal high calorie diet induces mitochondrial dysfunction and senescence phenotype in subcutaneous fat of newborn mice

Maternal high calorie diet induces mitochondrial dysfunction and senescence phenotype in subcutaneous fat of newborn mice

Fasting Drives Nrf2-Related Antioxidant Response in Skeletal Muscle

Browning of Adipose Tissue and Sirtuin Involvement

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