Short-term diet and moderate exercise in young overweight men modulate cardiocyte and hepatocarcinoma survival by oxidative stress.
Marcellino MondaGiovanni MessinaIlaria ScognamiglioAngela LombardiGiuseppe A MartinPasquale SperlonganoMarina PorcelliMichele CaragliaPaola StiusoPublished in: Oxidative medicine and cellular longevity (2014)
The present study was designed to evaluate the effects of diet lifestyle on extending lifespan and reducing liver cancer risk. Young overweight men (n = 20), without metabolic syndrome, were placed in a 3-week residential program on a low-fat diet and moderate aerobic exercise. In each subject, pre- and postintervention fasting blood were collected for evaluating levels of serum lipids, and oxidative stress markers. Using subject sera and cardiomyocyte (H9C2) culture systems, we measured heat shock protein 27 and 90 expression, lipid accumulation, and oxidative stress marker levels. After 3-weeks of diet, significant reductions (P < 0.05) in body mass index, serum lipids and lipid ratios, and oxidative markers were recorded. In vitro, we observed that the addition of postintervention sera increased H9C2 cell number and reduced HSP27 and 90 expression, mitochondrial superoxide anion, and lipid accumulation with a parallel increase in nitric oxide (NO) production (all P < 0.01). At the same time, postintervention sera decreased human liver hepatocellular carcinoma cell line (HepG-2) proliferation, lipid accumulation, oxidative stress, and extracellular-signal-regulated kinases (ERK1/2) activity. Lifestyle modification in young overweight men, without metabolic syndrome, could ameliorate cardiocyte survival and reduce hepatocellular carcinoma cell proliferation.
Keyphrases
- oxidative stress
- weight loss
- physical activity
- metabolic syndrome
- heat shock protein
- middle aged
- body mass index
- cell proliferation
- nitric oxide
- dna damage
- poor prognosis
- high intensity
- heat shock
- weight gain
- induced apoptosis
- diabetic rats
- insulin resistance
- fatty acid
- ischemia reperfusion injury
- signaling pathway
- hydrogen peroxide
- binding protein
- adipose tissue
- randomized controlled trial
- cardiovascular disease
- stem cells
- cell cycle
- glycemic control
- endothelial cells
- pi k akt
- air pollution
- type diabetes
- cell therapy
- cardiovascular risk factors
- ionic liquid
- long non coding rna
- blood glucose
- mesenchymal stem cells
- heat stress
- resistance training
- angiotensin ii
- endoplasmic reticulum stress