“Four weeks of dietary CoQ10 in HM pigs enhances active, nuclear-bound PGC1α and increases the expression of ETC proteins within mitochondria of HM tissue.”
“Fatty liver, or hepatic steatosis, which develops when the body produces too much fat or doesn’t metabolize fat efficiently enough, affects around 25% of the global population. Excess fat is stored in liver cells, where it accumulates and can cause fatty liver and other diseases.
In a study just published in the journal Cell Reports, researchers reveal for the first time that SIRT6, a protein involved in regulating many biological processes such as aging, obesity, insulin resistance, inflammation and metabolism, also plays a crucial role in burning and regulating liver fat metabolism.”
“High protein intake, partly mediated by energy intake, may delay incident frailty in very old adults. Frailty prevention strategies in this age group should consider adequate provision of protein and energy.”
“Fundamental cellular mechanisms such as nutrient sensing, DNA damage response pathways, and cell cycle regulation influence the aging process. Studies have shown that the nutrient sensory kinase, mTOR (TOR in yeast), regulates lifespan in response to nutrient availability. The mTOR kinase forms two distinct protein complexes: TORC1 and TORC2. TORC1, which is inhibited by rapamycin, regulates cell growth, proliferation, and metabolism. It is well established that TORC1 promotes protein translation via phosphorylation of ribosomal protein S6 kinase and the eIF4Eâ€binding protein (BP; Zoncu, Efeyan, & Sabatini, 2011). The TORC2 branch is less studied; however, TORC2 also plays important roles in metabolism, cell survival, and proliferation (Zoncu et al., 2011). Although the involvement of the TORC1 pathway in lifespan regulation is conserved among many species (i.e., TORC1 inhibition extends lifespan), it is still unclear how this pathway affects multiple downstream stress and damage response mechanisms.”
“The AMP-activated protein kinase (AMPK) acts as a cellular energy sensor. Once switched on by increases in cellular AMP : ATP ratios, it acts to restore energy homeostasis by switching on catabolic pathways while switching off cell growth and proliferation. The canonical AMP-dependent mechanism of activation requires the upstream kinase LKB1, which was identified genetically to be a tumour suppressor. AMPK can also be switched on by increases in intracellular Ca2+, by glucose starvation and by DNA damage via non-canonical, AMP-independent pathways. Genetic studies of the role of AMPK in mouse cancer suggest that, before disease arises, AMPK acts as a tumour suppressor that protects against cancer, with this protection being further enhanced by AMPK activators such as the biguanide phenformin. However, once cancer has occurred, AMPK switches to being a tumour promoter instead, enhancing cancer cell survival by protecting against metabolic, oxidative and genotoxic stresses. Studies of genetic changes in human cancer also suggest diverging roles for genes encoding subunit isoforms, with some being frequently amplified, while others are mutated.”
“These studies demonstrate an important link between the [pathological] accelerated ageing process and normal aging, and also expose the CSB protein as a key factor against cellular ageing” concludes Dr. Ricchetti.
https://medicalxpress.com/news/2019-12-identification-key-protein-linked-ageing.html