Overnutrition and its sequelae have become a global concern due to the increasing inci- dence of obesity and insulin resistance. A ketogenic diet (KD) is widely used as a dietary treatment for metabolic disorders. Sirtuin1 (SIRT1), a metabolic sensor which regulates fat homeostasis, is modulated by dietary interventions. However, the influence of nutritional ketosis on SIRT1 is still debated. We examined the effect of KD on adipose tissue, liver, and serum levels of SIRT1 in mice. Adult C57BL/6J male mice were randomly assigned to two isocaloric dietary groups and fed with either high-fat KD or normal chow (NC) for 4 weeks. Serum SIRT1, beta-hydroxybutyrate (βHB), glucose, and triglyceride levels, as well as SIRT1 expression in visceral (VAT), subcutaneous (SAT), and brown (BAT) adipose tissues, and in the liver, were measured. KD-fed mice showed an increase in serum βHB in parallel with serum SIRT1 (r = 0.732, p = 0.0156), and increased SIRT1 protein ex- pression in SAT and VAT. SIRT1 levels remained unchanged in BAT and in the liver, which devel- oped steatosis. Normal glycemia and triglycerides were observed. Under a KD, serum and white fat phenotypes show higher SIRT1, suggesting that one of the molecular mechanisms underlying a KD’s potential benefits on metabolic health involves a synergistic interaction with SIRT1.

Ketogenic Diet Increases Serum and White Adipose Tissue SIRT1 Expression in Mice / Tozzi, Rossella; Campolo, Federica; Baldini, Enke; Venneri, MARY ANNA; Lubrano, Carla; Ulisse, Salvatore; Gnessi, Lucio; Mariani, Stefania. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1422-0067. - 23:24(2022). [10.3390/ijms232415860]

Ketogenic Diet Increases Serum and White Adipose Tissue SIRT1 Expression in Mice

Rossella Tozzi
Co-primo
;
Federica Campolo
Co-primo
;
Enke Baldini;Mary Anna Venneri;Carla Lubrano;Salvatore Ulisse;Lucio Gnessi;Stefania Mariani
Ultimo
2022

Abstract

Overnutrition and its sequelae have become a global concern due to the increasing inci- dence of obesity and insulin resistance. A ketogenic diet (KD) is widely used as a dietary treatment for metabolic disorders. Sirtuin1 (SIRT1), a metabolic sensor which regulates fat homeostasis, is modulated by dietary interventions. However, the influence of nutritional ketosis on SIRT1 is still debated. We examined the effect of KD on adipose tissue, liver, and serum levels of SIRT1 in mice. Adult C57BL/6J male mice were randomly assigned to two isocaloric dietary groups and fed with either high-fat KD or normal chow (NC) for 4 weeks. Serum SIRT1, beta-hydroxybutyrate (βHB), glucose, and triglyceride levels, as well as SIRT1 expression in visceral (VAT), subcutaneous (SAT), and brown (BAT) adipose tissues, and in the liver, were measured. KD-fed mice showed an increase in serum βHB in parallel with serum SIRT1 (r = 0.732, p = 0.0156), and increased SIRT1 protein ex- pression in SAT and VAT. SIRT1 levels remained unchanged in BAT and in the liver, which devel- oped steatosis. Normal glycemia and triglycerides were observed. Under a KD, serum and white fat phenotypes show higher SIRT1, suggesting that one of the molecular mechanisms underlying a KD’s potential benefits on metabolic health involves a synergistic interaction with SIRT1.
2022
SIRT1; ketogenic diet; ketone bodies; obesity; epigenetic regulators; adipose tissue
01 Pubblicazione su rivista::01a Articolo in rivista
Ketogenic Diet Increases Serum and White Adipose Tissue SIRT1 Expression in Mice / Tozzi, Rossella; Campolo, Federica; Baldini, Enke; Venneri, MARY ANNA; Lubrano, Carla; Ulisse, Salvatore; Gnessi, Lucio; Mariani, Stefania. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1422-0067. - 23:24(2022). [10.3390/ijms232415860]
File allegati a questo prodotto
File Dimensione Formato  
Tozzi_Ketogenic-Diet_2022.pdf

accesso aperto

Tipologia: Documento in Post-print (versione successiva alla peer review e accettata per la pubblicazione)
Licenza: Creative commons
Dimensione 696.05 kB
Formato Adobe PDF
696.05 kB Adobe PDF

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1662449
Citazioni
  • ???jsp.display-item.citation.pmc??? 0
  • Scopus 0
  • ???jsp.display-item.citation.isi??? 0
social impact