How to Improve Metabolic Health: Neurophysiology, Part 1

How to Improve Metabolic Health: Neurophysiology, Part 1: Nuclear factor-Kappa B (NF-KB) represents a family of inducible transcription factors, which regulates a large array of genes involved in different processes of the immune and inflammatory responses.

The NF-KB proteins are normally sequestered in the cytoplasm by a family of inhibitory proteins, including IKB family members and related proteins characterized by the presence of ankyrin repeats. To date, the best studied and most important IKB family member is IKBa.

The activation of NF-KB involves two major signaling pathways, canonical and noncanonical, are important for regulating immune and inflammatory responses, despite their differences in signaling mechanism. The canonical NF-KB pathway responds to diverse stimuli, including TNF receptor superfamily members, T-cell receptors, and B cell receptors. In contrast to the canonical NF-KB pathway, the noncanonical NF-KB pathway selectively responds to a specific group of stimuli, including ligands of a subset of TNFR superfamily members.

A large body of literature supports the idea that nuclear factor kappa B (NF-KB) signaling contributes to not only immunity, but also inflammation, cancer, and nervous system function.

Functionally, canonical NF-KB is involved in almost all aspects of immune responses, whereas the noncanonical NF-KB pathway appears to be evolved as a supplementary signaling axis that cooperates with canonical NF-KB pathway in the regulation of specific functions of the adaptive immune system. A well-recognized function of NFKB is regulation of inflammatory responses and the activation, differentiation and effector function of inflammatory T cells.

Mammals have three mostly nuclear Sirtuin isoforms (SIRT-1, 6, & 7), one cytosolic (SIRT-2), and three mitochondrial (SIRT-3, 4, & 5), although additional localizations have been described for several of these isoforms.

SIRT-1, 6, & 7: Regulate DNA homeostasis.
SIRT-2: Regulates cell cycle progression.
SIRT-3 (mitochondrial): Regulates a wide range of targets from signaling proteins to metabolic enzymes. It has been implicated in responses to exercise or nutritional regime, in aging-related disorders such as type II diabetes and cardiovascular diseases, and in caloric restriction.
SIRT-4 (mitochondrial): Regulates metabolic enzymes, and has been implicated in metabolic disorders.
SIRT-5 (mitochondrial): Regulates metabolic enzymes and stress response proteins, has been implicated in metabolic adaptations to protein-rich diet, fasting, and long-term caloric restriction, and seems to contribute to repairing metabolic dysfunction and neurodegeneration.

Activation of SIRT-3 and SIRT-5 could be attractive for treatment of cancer, heart failure and metabolic dysfunction. Increased SIRT-3 activity has shown to block and reverse cardiac hypertrophy in mice, reduced β-Amyloid in vitro, and alleviated cognitive deficits of Alzheimer’s disease in mice. SIRT-5 activation might allow to prevent ischemia/reperfusion-induced oxidative injury. Recent findings underline that SIRT-5 is a potential suppressor of gastric cancer, pancreatic cancer, and possible other cancer types.

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