Principles of Nutrigenetics and Nutrigenomics by unknow

Principles of Nutrigenetics and Nutrigenomics by unknow

Author:unknow
Language: eng
Format: epub
Tags: Principles of Nutrigenetics and Nutrigenomics: Fundamentals of Individualized Nutrition, (2020) 588pp. 978-0-12-804572-5
ISBN: 5904579
Publisher: Elsevier Science & Technology
Published: 2019-09-20T23:33:02+00:00


NIACIN AND INFLAMMATION

291

regulating the expression of the key genes involved. In

SIRTs have a key role in regulating endothelial and

keeping with the protective role for promoting the effi-

vascular homeostasis. In the case of SIRT1, it has been

cient use of the limited resource, SIRT1 and SIRT2

demonstrated that increased NO production promotes

have been shown to inhibit adipogenesis. SIRT1 pro-

endothelial-dependent vasodilation by targeting endo-

motes adipogenesis inhibition as well as a switch from

thelial NO synthase and regulates the expression of

white fat adipocytes to metabolically active brown fat

many genes involved in vascular endothelial homeosta-

by inhibiting the transcription activity of the master

sis, angiogenesis signaling, and remodeling through the

regulator of adipogenesis PPARg. This mechanism in-

deacetylation of FOXO1.

volves direct deacetylation of PPARg and binding of

SIRT1 with the PPARg corepressors nuclear receptor

corepressor and silencing mediator of retinoid and thy-

NIACIN AND VASCULAR HOMEOSTASIS

roid hormone receptors. SIRT1 has also been implicated

in NASH, because Sirt1/ mice were found to be more

As a consequence of the hypolipidemic effects of

prone to developing hepatic steatosis than were wild-

niacin, reduced thrombocyte aggregation and blood vis-

type animals. The involvement of SIRT2 has been associ-

cosity have also been observed. Niacin treatment using

ated with the modulation of transcription factor FOXO1

HepG2 cells lowers plasminogen activator inhibitor-1,

activity, altering the expression of regulators PPARg,

a factor possibly involved in atherogenesis and throm-

CCAAT-enhancer-binding protein a, and causing the

bosis, and intercellular adhesion molecule 1 levels, a

repression of markers of terminal adipocyte differentia-

cell surface glycoprotein important for the adhesion of

tion, such as Glut4, aP2, and fatty acid synthase. In

white blood cells to vascular surfaces, and which has

contrast, mitochondrial SIRT3 and SIRT5 promote fatty

significant properties as a predictor of future coronary

acid b-oxidation by regulating pyruvate dehydrogenase.

events (Tavintharan et al., 2007). Interestingly, among

SIRT6 has also been linked to fatty acid synthesis inhibi-

the SIRT family, SIRT1 is the only one reported to control

tion, because fatty acid transport and lipogenesis are

angiogenesis

signaling,

by

modulating

postnatal

induced in Sirt6/ livers in mice. Hepatic SIRT7 has

vascular growth through FOXO1 deacetylation.

been proposed to have a role opposite the other SIRTs

in lipid metabolism, in which SIRT7 promotes the

expression of genes involved in fatty acid uptake and

NIACIN AND ISCHEMIA

synthesis of triglycerides by inhibiting DCAF1/DDB1/

CUL4B E3-dependent polyubiquitination of transcrip-

An interesting link was established between niacin

tion factor TR4. Consistently, Sirt7/ mice accumulate

administration and the attenuation of reperfusion

less body fat and are more resistant to developing

injury; tissue damage occurs when blood flows into

high-fat dieteinduced obesity.

the tissue after a period of ischemia. Niacin treatment

leads to improved kidney ischemia-reperfusion (I/R)-

induced cardiac dysfunction and the severity of

NIACIN IN ENDOTHELIAL

myocardial LPO through sustained myocardial PGC-

DYSFUNCTION

1a expression. I/R injury can also be suppressed by

SIRT1 or SIRT6, whose functions either induce auto-

Endothelial dysfunction is a condition characterized

phagy in liver or are essential to ensure the sodium

by an imbalance between vasodilating and vasocon-

sulfideemediated cytoprotective effect in brain endo-

stricting substances produced by endothelial cells, which

thelial cells, respectively. Whereas SIRT1 and SIRT6 sup-

may result in raised blood pressure, reduced vasodila-

press I/R injury, SIRT2 inhibition and/or depletion in

tion, and proinflammatory and prothrombotic states.

mice promote protection from ischemic injury.

Niacin can improve endothelial function under vascular

injury and endothelial tube formation under lipotoxic

and hypoxic conditions, which are



Download



Copyright Disclaimer:
This site does not store any files on its server. We only index and link to content provided by other sites. Please contact the content providers to delete copyright contents if any and email us, we'll remove relevant links or contents immediately.