**5. Conclusions**

Metainflammation can be defined as the systemic metabolic inflammation derived from obese adipose tissue in which innate and adaptive immune system cells have changed in number and function, from a lean and homeostatic to a proinflammatory state, and whose cytokine and adipokine proinflammatory profiles cause metabolic syndrome. Some authors consider metainflammation as the result of dysfunctional adipose tissue that consists of unhealthy expansion (hypertrophy) and angiogenesis, hypoxia, and detrimental ECM remodeling, which in turn limit adipocyte lipid storage capacity; altogether, these deleterious scenarios cause lipolysis and ectopic fat accumulation in the liver and muscle.

The knowledge developed in recent years in relation to the homeostatic interaction between immune system and the energetic metabolism along with the role of miRs allows that in a state in imbalance such as obesity, new biomarkers that show clinical information about the state are sought health of individuals and the early detection of the risk of developing metabolic complications is derived from the state of pathological adiposity.

**25**

*Adipose Tissue in Health and Disease*

CDS critical death size CVD cardiovascular disease

DWAT dermal WAT ECM extracellular matrix

FFA free fatty acids

HFD high-fat diet

IL interleukin

miRs microRNAs

OPN osteopontin

SIRT 1 sirtuin 1

mRNA messenger RNAs MS metabolic syndrome MSCs mesenchymal stem cells

*DOI: http://dx.doi.org/10.5772/intechopen.90559*

CDK4 cyclin-dependent kinase 4

FGF21 fibroblast growth factor 21 FOXO1 forkhead box class O-1 Fstl 1 follistatin-related protein 1 G6PaseC glucose 6 phosphatase

GLUT transporter protein of glucose HDL high-density lipoproteins

HIF-1α hypoxia-inducible factor-1α HSL hormone sensitive lipase

ILC2 group 2 innate lymphoid cells

iNKT invariant natural killer T cells

IRS1 substrate of insulin receptor 1 IRS2 substrate of insulin receptor 2 KATP ATP-sensitive potassium channels

MCP-1 monocyte chemoattractant protein-1

NADH nicotinamide adenine dinucleotide in reduced form

MPK mitogen-activated protein kinase

PAI-1 plasminogen activator inhibitor-1 PCK1 phosphoenolpyruvate carboxy kinase

PDGFR platelet-derived growth factor receptor PEDF pigment epithelium-derived factor

RT-PCR real-time polymerase chain reaction

PPAR-γ peroxisome proliferator-activated receptor γ

SREBPs sterol regulatory element-binding proteins STAT3 signal transducer and activator of transcription 3

SPARC secreted protein, acidic, and rich in cysteine complex

PDGF platelet-derived growth factor

PI3K phosphoinositide 3-kinases

SCAT subcutaneous adipose tissue

SVF stromal-vascular fraction S1P sphingosine-1-phosphate TZD thiazolidinediones

IMCL intramolecular lipids

LDL low-density lipoprotein LPS lipopolysaccharide

NEFAS non-esterified fatty acids

PC pyruvate carboxylase

IR insulin resistance

ERK extracellular signal-regulated kinase-1 FADH flavin adenine dinucleotide in reduced form

## **Conflict of interest**

The authors declare no conflict of interest.


### **Acronyms and abbreviations**

#### *Adipose Tissue in Health and Disease DOI: http://dx.doi.org/10.5772/intechopen.90559*

*Obesity*

**5. Conclusions**

of pathological adiposity.

**Conflict of interest**

**Acronyms and abbreviations**

ADRB3 β3-adrenergic receptor AKT protein kinase B ASCs adipose stem cells AT adipose tissue

ATMs adipose tissue macrophages ATP adenosine triphosphate BAT brown adipose tissue

C/EBP-α CCAAT/enhancer-binding protein α

Furthermore, the other resident leucocytes will change in number and function as

The activation of NF-kB pathway with cytokine/chemokine release and the contribution of harmful metabolites (i.e., ceramide and sphingosine 1-phosphate, S1P) interfere with proper insulin signaling, therefore establishing a local AT IR [146–148]. After the AT IR is established, non-suppressive lipolysis now perpetuates and triggers high circulating FFA levels giving place to peripheral/systemic lipotoxicity: ectopic fat accumulation in liver and muscle; additionally, the proinflammatory cytokine, adipokine, and chemokine profile will circulate through the bloodstream, establishing metainflammation. Eventually, the high ectopic lipid concentration in this tissues will unleash similar detrimental effects that took place at AT, establish-

The ensemble of this AT dysfunction and its harmful metabolic clinical repercussions is what we call pathologic adiposity: the adiposity status that determinates metabolic systemic dysfunction (IR and dyslipidemia), whether in an obese or normal weight individual, "metabolically unhealthy obese" (MUO), or "metaboli-

Metainflammation can be defined as the systemic metabolic inflammation derived from obese adipose tissue in which innate and adaptive immune system cells have changed in number and function, from a lean and homeostatic to a proinflammatory state, and whose cytokine and adipokine proinflammatory profiles cause metabolic syndrome. Some authors consider metainflammation as the result of dysfunctional adipose tissue that consists of unhealthy expansion (hypertrophy) and angiogenesis, hypoxia, and detrimental ECM remodeling, which in turn limit adipocyte lipid storage capacity; altogether, these deleterious scenarios cause

The knowledge developed in recent years in relation to the homeostatic interaction between immune system and the energetic metabolism along with the role of miRs allows that in a state in imbalance such as obesity, new biomarkers that show clinical information about the state are sought health of individuals and the early detection of the risk of developing metabolic complications is derived from the state

ATMs did, towards a Th1-type immune response.

ing now peripheral/systemic IR and dyslipidemia [132, 149].

lipolysis and ectopic fat accumulation in the liver and muscle.

The authors declare no conflict of interest.

cally obese normal weight" (MONW) person, respectively (**Figure 3**).

**24**


#### *Obesity*

