asdsasa

1. MESOLIPOLISIS
• What we are targeting
• What cocktail we should give
• Another point of view regarding lipolisis
• Dr anggi yuliani utami,dipl.cos.med - LEMDIK

2. ADIPOSE TISSUE
ADIPOSE TISSUE AS A PSIKO NEURO IMUNO ENDOCRINE ORGAN

3. Target pencapaian

9. Stress manajemenet
Toxin manajemen
Alergy manajemen
Disbiosis manajemen- microbe
Malnutrition manajemen
GENE EXPRESSION

10. Adipose tissue

11. FUN FACT ABOUT ADIPOCYTES
• adipocytes are involved in the immune response, blood
pressure control, haemostasis, bone mass, and thyroid and
reproductive function
• synthesis and release of peptide hormones by adipocytes.
• Adipocytes also release fatty acids into the circulation, which
are used by most organs for fuel when glucose is limiting.
• Adipose tissue are psiko neuro imuno endocrine organ

12. Adipocytes are derived from
both resident mesenchymal
cells in the stromal-vascular
fraction of adipose tissue and
hematopoietic progenitors
that reside in the bone
marrow. In addition to
adipocytes, mesenchymal
progenitors can form other
connective tissue cells, such
as myocytes and osteocytes.
Myeloid progenitors derived
from hematopoietic
progenitors in bone marrow
give rise to adipocytes as well
as neutrophils, macrophages,
dendritic cells, and
granulocytes.

14. ANATOMI – BIOLOGI CELL

22. TYPE OF ADIPOSE TISSUE

24. LOCATION
• Adipose tissue is commonly known as body fat. It is found all
over the body. It can be found under the skin (subcutaneous
fat), packed around internal organs (visceral fat), between
muscles, within bone marrow and in breast tissue.

25. The diverse distribution of white adipose tissue.
There are several white adipose depots
distributed throughout the human body that
include, but are not limited to, dermal adipose
tissue, epicardial adipose tissue, perinodal
adipose tissue, mammary adipose tissue,
subcutaneous adipose tissue, and visceral
adipose tissue.

29. VERTICAL ANATOMY OF ADIPOSE TISSUE
AROUND BODY
• face
• Double chin
• Lengan
• Paha
• perut

30. • the presence of mature adipocytes within skeletal muscle. This
occurs under some pathological conditions (i.e., primary
myodystrophies, obesity, hyperglycemia, high plasma free fatty
acids, hypoxia, etc.) or as a consequence of thiazolidinedione
treatment or simply because of a sedentary lifestyle or during
aging.
• Several pathways and factors (PPARs, WNT growth factors,
myokines, GEF-GAP-Rho, p66shc, mitochondrial ROS
production, PKCβ) could be implicated in the adipogenic
conversion of SCs. The understanding of the molecular
pathways that regulate muscle-to-fat conversion and SC
behavior could explain the increase in IMAT depots that
characterize many metabolic diseases and age-related
sarcopenia.

31. • The sources of adipocytes may be also lungs, bone marrow and
blood vessels adventitia. Adipokines – a protein mediators; are
secreted by adipocytes, macrophages, peripheral blood
mononuclear cells, endothelial cells

32. • The color yellow was assigned to marrow adipose tissue
• (MAT) (Fig. 1). In a healthy, lean person, MAT represents
• over 10% of total fat mass [13]. Although adipocytes of the
• BM resemble the white adipocyte’s unilocular morphology,
• they display a distinct gene expression [14], lipid profile
• [14, 15] and metabolism, e.g., seem to be resistant to calorie
• restriction-induced hydrolysis of stored triglycerides

33. WHITE ADIPOSE TISSUE DISTRIBUTION
white adipose tissue is divided into subcutaneous adipose
tissue (SAT), mainly localised in the gluteus, thighs
and abdomen and visceral adipose tissue (VAT), also known
as
intra-abdominal fat, mostly composed of mesenteric and
omental fat. In healthy subjects, the SAT deposits correspond
to 80%
of total fat mass, whilst the VAT deposits correspond to 10–
20%
(Oka et al. 2010). The VAT compared with the SAT is more
cellular, innervated and vascularised (Gealekman et al. 2011;
Villaret et al. 2010); contains more leukocytes; and is also
more
metabolically active, having distinct adipokine secretion
profiles
(Ibrahim 2010). These divergences might be, at least in part,
explained by different embryonic origins, as suggested by
recent

34. LYMPHATIC SYSTEM AND ADIPOSE TISSUE
• The lack of adequate lymphatic drainage in lymphedema is
• considered one of the main causes of SAT expansion observed
in
• the affected areas (Warren et al. 2007). Additionally, it was
observed that a high-fat diet induces lymphatic dysfunction
accompanied by capillary dilation in the dermis and reduction
of the
• contractile function of collecting vessels (Aschen et al. 2012;
• Blum et al. 2014; Sawane et al. 2013; Weitman et al. 2013)

35. • Lymphatic vessels are abundant in human VAT but are rare in
SAT.
• lymph vessels were clearly observed in the interlobular fibrous
septa, in the fibrous septa crossing the adipose parenchyma, as
well as in association with the subcutaneous vascular plexus.
These results are in accordance with morphological studies
from Ryan
• (1989, 1995), who described lymphatic vessels only in the SAT
borders, as well as with updated studies on dermal
microcirculation, in which lymphatic capillaries remain mostly
unreported (Breslin et al. 2019), despite eventual imaging of
collecting lymphatics in the SAT (Tashiro et al. 2017)

39. ADIPOSE TISSSUE AND ORGAN
COMMUNICATION
Fat tissue can ‘talk' to other organs

43. ADIPOSE AND COMPLEMENT
• Adipose tissue synthesizes complement proteins and is a target
of complement activation. C3a-desArg/acylation-stimulating
protein stimulates lipogenesis and affects lipid metabolism.

45. ADIPOSE TISSUE AS AN IMMUNOLOGICAL
ORGAN: TOLL-LIKE RECEPTORS, C1Q/TNFS
AND CTRPS

46. ADIPOSITE AND CELLULAR RESPON
IMMUNE
The role of adipocytes in adaptive
immunity. Adipocytes express MHC
class II molecules and several T cell
costimulators to act as antigen-
presenting cells (APCs), and induce the
activation of CD4+ T cells in visceral
adipose tissue during obesity. In
addition, adipocytes secrete various
adipokines, including leptin,
adiponectin, IL-6, TNF-α, resistin, and
visfatin, to regulate the proliferation
and differentiation of T cells. In B cell-
mediated humoral immunity, adipocytes
modulate B cell generation,
development, aging, activation and
antibody production mainly by secreting
adipokines, including leptin,

47. ADIPOSE TISSUE AS AN ENDOCRINE ORGAN.

49. • Why we accumulate fat excessively
The excessive accumulation of fat in certain areas of the body, which
ends up being unsightly, has not so much to do with the amount of fat
contained in the food we eat but with the excess energy that we
provide to our body. As we have seen, adipocytes are responsible for
both storing fat and mobilizing it. Whether one or another process
occurs will depend on the energy required by our body. Therefore, if
we want to avoid excessive fat accumulation, it is very important to
find a balance between the different factors (internal and external) that
influence the configuration of our adipocytes: physical activity, toxic
habits, hormones, genetics, age, rest, feeding, etc.

57. MESOTHERAPY
• Mesotherapy is a form of medical therapy popular in Europe and South America. It is used for treating
a variety of medical conditions, including the treatment of localized fat deposits and cellulite.
Phosphatidylcholine/deoxycholate injections are a popular technique to treat localized fat
accumulations and have recently become synonymous with mesotherapy, although their history and
technique are distinct. To treat localized fat deposits, phosphatidylcholine (PC) and deoxycholate (DC)
are utilized. To date, there have been no published histological studies that explain the mechanism of
action of PC and DC.Method. In this study the authors have obtained skin biopsies from a patient who
had undergone mesotherapy with PC and DC. Punch biopsies were taken at one and two weeks after
the procedure.Results. Each of the biopsies taken at one and two weeks after treatment with PC and
DC showed a normal epithelium and dermis, with a mixed septal and lobular panniculitis. The fat
lobules were infiltrated by increased numbers of lymphocytes and, in particular, macrophages. The
macrophages consisted of conventional forms, foam cells, and multinucleated fat-containing giant
cells. The inflammation was associated with serous atrophy and microcyst formation.Conclusion. This
study demonstrates that mesotherapy with PC and DC affects the subcutaneous fat. We theorize that
the reduction of subcutaneous fat likely follows inflammatory-mediated necrosis and resorption.
• Histological changes associated with mesotherapy for fat dissolution .2005 .Paul T Rose 1, Michael
Morganhttps://pubmed.ncbi.nlm.nih.gov/16020211/

58. DWAT
• Dermal white adipose tissue is a unique layer of adipocytes
within the reticular dermis of the skin. Recently, several
nonmetabolic activities have been discovered for dWAT and its
fibroblast precursors. These functions include antimicrobial
defense and roles in hair cycling, wound healing, and
thermogenesis.

59. • Physiological role of adipose tissue: white adipose tissue as an
endocrine and secretory organ
• The metabolic role of white fat is, however, complex.

60. • Leptin is one of a number of proteins secreted from white adipocytes, which
include angiotensinogen, adipsin, acylation-stimulating protein, adiponectin,
retinol-binding protein, tumour neorosis factor a, interleukin 6, plasminogen
activator inhibitor-1 and tissue factor. Some of these proteins are inflammatory
cytokines, some play a role in lipid metabolism, while others are involved in
vascular haemostasis or the complement system. The effects of specific proteins
maybe autocrine or paracrine, or the site of action maybe distant from adipose
tissue. The most recently described adipocyte secretory proteins are fasting-
induced adipose factor, a fibrinogen-angiopoietin-related protein,
metallothionein and resistin. Resistin is an adipose tissue-specific factor which
is reported to induce insulin resistance, linking diabetes to obesity.
Metallothionein is a metal-binding and stress-response protein which may have
an antioxidant role. The key challenges in establishing the secretory functions of
white fat are to identify the complement of secreted proteins, to establish the
role of each secreted protein, and to assess the pathophysiological
consequences of changes in adipocyte protein production with alterations in
adiposity (obesity, fasting, cachexia). There is already considerable evidence of
links between increased production of some adipocyte factors and the metabolic
and cardiovascular complications of obesity. In essence, white adipose tissue is
a major secretory and endocrine organ involved in a range of functions beyond
simple fat storage.

61. • in the obese state, hypertrophic adipocytes and activated
macrophages produce decreased level of adiponectin and
increased levels of pro-inflammatory adipokines and cytokines
leading to “metabolic inflammation”. It may be possible that
these obesity-related pro-inflammatory adipokines may be
associated with airway inflammation in obesity-related asthma.

62. • adipokine between subcutaneous and visceral adipose tissue
that are characterized by unique profile of adipokine
production. In the visceral tissue, higher levels of PAI-1 and IL-
6 have been identified. On the other hand, the higher levels of
adiponectin and leptin have been observed in the subcutaneous
tissue
• The expression and the activity of these enzymes are regulated
by different hormones and growth factors, such as insulin,
leptin, and adiponectin.

63. • aging dWAT, impaired collagen biosynthesis, angiogenesis, and
melanin synthesis were identified.
• skin that has been chronically photo-damaged displays a
reduction of the dWAT volume, caused by the replacement of
adipocytes by fibrotic structures.
• prevalence of hypertrophic scarring and the appearance of
signs of skin aging in different ethnic groups. These
observations could elevate dermal adipocytes to prime targets
in strategies aimed at counteracting skin aging.

64. • white adipose tissue (WAT) secretes a number of peptide
hormones, including leptin, several cytokines, adipsin and
acylation-stimulating protein (ASP), angiotensinogen,
plasminogen activator inhibitor-1 (PAI-1), adiponectin, resistin
etc., and also produces steroids hormones. This newly
discovered secretory function has shifted our view of WAT,
which is no longer considered only an energy storage tissue but
a major endocrine organ, at the heart of a complex network
influencing energy homeostasis, glucose and lipid metabolism,
vascular homeostasis, immune response and even reproduction

65. • adipose secreted proteins are dysregulated when the WAT
mass is markedly altered, either increased in the obese state or
decreased in lipoatrophy.
• adipose-secreted products in the ethiopathology and/or
complications of both obesity and cachexia.
• adipose secretion by focusing on protein and steroid
hormones. Regulation of WAT secretion by the major regulatory
factors impinging on the adipocytes, i.e. insulin,
glucocorticoids, catecholamines

66. White adipose tissue
• There are two types of adipose tissue: BAT or brown adipose
tissue and WAT or white adipose tissue. BAT in humans
surrounds the heart and great vessels in infancy and tends to
disappear as the individual grows. WAT, on the other hand, is
the largest store of lipids incorporated through daily intake.
The volume of white adipose tissue (WAT) depends on the
number of adipocytes and their size, so its growth may be due
to an increase in the number of adipocytes or to an increase in
their lipid content.

67. AGING AND ADIPOCYTES
• Aging is accompanied by a loss of classical brown adipocytes as well
as the brown-like adipocytes found in white adipose tissue,
suggesting that loss of their energy-expending capacity might
contribute to an obesity-prone phenotype with increased age.
• Beige or brite (brown-in-white) adipocytes are present in white
adipose tissue (WAT) and have a white fat-like phenotype that when
stimulated acquires a brown fat-like phenotype, leading to increased
thermogenesis. This phenomenon is known as browning and is more
likely to occur in subcutaneous fat depots

68. • subcutaneous injections of a formula containing phosphatidylcholine
combined with its emulsifier, deoxycholate, are effective in removing
small collections of adipose tissue. Cell lysis, resulting from the
detergent action of deoxycholate, may account for this clinical effect.
• Dermatol Surg
• . 2006 Apr;32(4):465-80. doi: 10.1111/j.1524-4725.2006.32100.x.
• Mesotherapy and phosphatidylcholine injections: historical
clarification and review
• Adam M Rotunda 1, Michael S Kolodney

69. • We propose that lipolysis in adipose tissue mainly impacts lipid
accumulation and obesity in the body, but not on glucose
metabolism. In general, activation of the sympathetic system
and the downstream adrenergic receptors in adipose tissue can
stimulate both lipolysis and thermogenesis

71. • Adipose tissue is composed of adipose stem cells (the precursor cells that
give rise to new adipocytes), adipocytes (the fat-storing cells) and various
other cell types, which include mural, endothelial and neuronal cells.
• Distinct developmental origins contribute to white adipose tissue (WAT) and
brown adipose tissue (BAT) in mice.
• In the trunk, white adipocytes arise from adipocyte progenitor cells (APs)
present in the mural wall of WAT blood vessels (truncal WAT). These APs
could stem from lateral mesoderm-derived mesenchymal stem cells (MSCs),
which originate from a common endothelial and mesenchymal cell precursor
which also gives rise to the subcutaneous progenitor population. In
contrast,,white adipose depots in the head originate from the cranial neural
crest, and not the mesoderm progenitors. BAT and skeletal muscles share a
common developmental origin, which is distinct from WAT. They originate
from paraxial mesoderm-derived progenitor cells residing in the
dermomyotome, a somite sub-domain. It is assumed that some WAT
progenitor cells can transdifferntiate to give rise to 'brown'-like progenitor
cells.