Treating Metabolic Dysregulation and Senescence by Caloric Restriction: Killing Two Birds with One Stone? DOI Creative Commons
Lara Russo, Serena Babboni, Maria Grazia Andreassi

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(1), P. 99 - 99

Published: Jan. 16, 2025

Cellular senescence is a state of permanent cell cycle arrest accompanied by metabolic activity and characteristic phenotypic changes. This process crucial for developing age-related diseases, where excessive calorie intake accelerates dysfunction aging. Overnutrition disturbs key pathways, including insulin/insulin-like growth factor signaling (IIS), the mammalian target rapamycin (mTOR), AMP-activated protein kinase. The dysregulation these pathways contributes to insulin resistance, impaired autophagy, exacerbated oxidative stress, mitochondrial dysfunction, further enhancing cellular systemic derangements. On other hand, dysfunctional endothelial cells adipocytes contribute inflammation, reduced nitric oxide production, altered lipid metabolism. Numerous factors, extracellular vesicles, mediate pathological communication between vascular system adipose tissue, amplifying imbalances. Meanwhile, caloric restriction (CR) emerges as potent intervention counteract overnutrition effects, improve function, reduce restore balance. CR modulates such IIS, mTOR, sirtuins, glucose metabolism, reducing promoting autophagy. can extend health span mitigate diseases delaying improving healthy endothelial-adipocyte interactions. review highlights crosstalk adipocytes, emphasizing potential in counteracting overnutrition-induced restoring homeostasis.

Language: Английский

Age-specific and sex-specific associations of visceral adipose tissue with metabolic health status and cardiovascular disease risk DOI
Wenhao Zhang, Xiangqian Su,

SiHua Liu

et al.

Acta Diabetologica, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 10, 2025

Language: Английский

Citations

1
A nutrigeroscience approach: Dietary macronutrients and cellular senescence DOI
Mariah F. Calubag, Paul D. Robbins, Dudley W. Lamming

et al.

Cell Metabolism, Journal Year: 2024, Volume and Issue: 36(9), P. 1914 - 1944

Published: Aug. 23, 2024

Language: Английский

Citations

5
The Roles of White Adipose Tissue and Liver NADPH in Dietary Restriction-Induced Longevity DOI Creative Commons

Leah E. Jamerson,

Patrick C. Bradshaw

Antioxidants, Journal Year: 2024, Volume and Issue: 13(7), P. 820 - 820

Published: July 8, 2024

Dietary restriction (DR) protocols frequently employ intermittent fasting. Following a period of fasting, meal consumption increases lipogenic gene expression, including that NADPH-generating enzymes fuel lipogenesis in white adipose tissue (WAT) through the induction transcriptional regulators SREBP-1c and CHREBP. knockout mice, unlike controls, did not show an extended lifespan on DR diet. WAT cytoplasmic NADPH is generated by both malic enzyme 1 (ME1) pentose phosphate pathway (PPP), while liver primarily synthesized folate cycle provided one-carbon units serine catabolism. During daily fasting diet, fatty acids are released from transported to peripheral tissues, where they used for beta-oxidation phospholipid lipid droplet synthesis, monounsaturated (MUFAs) may activate Nrf1 inhibit ferroptosis promote longevity. Decreased PPP stimulated browning protected high-fat high levels macrophages linked obesity. But oscillations [NADPH]/[NADP+] feeding cycles play important role maintaining metabolic plasticity drive Studies measuring malate/pyruvate as proxy [NADPH]/[NADP+], well studies using fluorescent biosensors expressed animal models monitor changes needed during ad libitum diets determine associated with

Language: Английский

Citations

3
Treating Metabolic Dysregulation and Senescence by Caloric Restriction: Killing Two Birds with One Stone? DOI Creative Commons
Lara Russo, Serena Babboni, Maria Grazia Andreassi

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(1), P. 99 - 99

Published: Jan. 16, 2025

Cellular senescence is a state of permanent cell cycle arrest accompanied by metabolic activity and characteristic phenotypic changes. This process crucial for developing age-related diseases, where excessive calorie intake accelerates dysfunction aging. Overnutrition disturbs key pathways, including insulin/insulin-like growth factor signaling (IIS), the mammalian target rapamycin (mTOR), AMP-activated protein kinase. The dysregulation these pathways contributes to insulin resistance, impaired autophagy, exacerbated oxidative stress, mitochondrial dysfunction, further enhancing cellular systemic derangements. On other hand, dysfunctional endothelial cells adipocytes contribute inflammation, reduced nitric oxide production, altered lipid metabolism. Numerous factors, extracellular vesicles, mediate pathological communication between vascular system adipose tissue, amplifying imbalances. Meanwhile, caloric restriction (CR) emerges as potent intervention counteract overnutrition effects, improve function, reduce restore balance. CR modulates such IIS, mTOR, sirtuins, glucose metabolism, reducing promoting autophagy. can extend health span mitigate diseases delaying improving healthy endothelial-adipocyte interactions. review highlights crosstalk adipocytes, emphasizing potential in counteracting overnutrition-induced restoring homeostasis.

Language: Английский

Citations

0