Subcutaneous fat Adipose tissue anatomy


Factors that stimulate adipogenesis



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Factors that stimulate adipogenesis

Glucocorticoids (GCs) are potent inducers of adipogenesis in vitro, and hypercortisolism is associated with obesity and disturbances in fat tissue distribution. GC receptors are present in human pre-adipocytes, and GCs activate the expression of C/EBP-δ and PPAR-γ (Joyner et al., 2000).

Ingestion of a high-fat diet, particularly a diet rich in saturated fatty acids, induces hypertrophy and hyperplasia of adipose tissue. Polyunsaturated fatty acids, which are less potent for increasing the number of adipocytes in vivo, are more effective than saturated fatty acids in stimulating pre-adipocyte differentiation in culture; an effect probably related to the ability of polyunsaturated fatty acids to act as ligands or precursors of ligands for PPAR- γ (Sweeney et al., 1999).


Balance between pro- and anti-adipogenic environmental factors and pathways. Reproduce 12 cm wide (Bruno, 2005).

Insulin favors fat storage by increasing LPL and decreasing HSL activity. Insulin has stronger antilipolytic effects in adipose located in the abdominal region compared to the femoral regions in both men and women. Paradoxically, insulin binding is stronger in the gluteal–femoral region than the abdominal region (Sweeney et al., 1999).


Some prostaglandins positively regulate adipogenesis. Prostacyclin (PGI2) stimulates adipogenesis by binding to the prostanoid G-protein-coupled receptors on pre-adipocytes. The consecutive increase in intracellular cAMP mediates the rapid induction of C/EBP-β and -δ by PGI2. Moreover, PGI2 might stimulate adipose conversion by its ability to bind and activate the PPAR-γ nuclear receptor. D-Prostaglandin J2 (PGJ2), through its potential binding to PPAR- γ, also promotes adipogenesis (Aubert et al., 2000).
Adiponectin is secreted from adipocytes, and low circulating levels have been associated with obesity, insulin resistance, type 2 diabetes and cardiovascular diseases. Pre-adipocyte cell lines overexpressing adiponectin differentiate into adipocytes more rapidly, and exhibit more prolonged and strong gene expression for key adipogenic transcription factors, as well as increased insulin responsiveness, during adipose conversion (Fu et al., 2005).

Factors that inhibit adipogenesis
Inflammatory cytokines, including tumour necrosis factor-α (TNF-α), interleukin-1, IL-6, IL-11, leukaemia inhibitory factor, interferon-γ, oncostatin M and ciliary neurotrophic factor, can inhibit stem cell commitment and differentiation, or even induce dedifferentiation. These cytokines might play a role in lipoatrophy connected to cancer cachexia and inflammatory and chronically infectious diseases (Suzawa et al., 2003).

Growth hormone (GH) has been shown to decrease adiposity in vivo, and this is likely to be essentially due to the stimulation of lipolysis. In addition, GH displays inhibitory effects on pre-adipocyte differentiation in culture, suggesting that a limitation in adipogenesis could be involved in the GH-induced reduction in fat depots. However, this is in contrast with the observation that GH stimulates the adipose conversion of several embryonically derived pre-adipocyte cell lines, and suggests that the latter models reflect earlier developmental stages (Wabitsch et al., 1995).


Resistin is another adipose-secreted protein that represents a potential link between obesity and insulin resistance in rodents. Mice lacking resistin exhibit increased insulin sensitivity. Moreover, resistin is able to inhibit adipogenesis (Banerjee et al., 2004).
The Wnt family of secreted glycoproteins acts through autocrine or paracrine mechanisms to influence the development of many cell types. Ectopic expression of the Wnt1 gene potently represses adipogenesis. Wnt completely blocks induction of the key adipogenic transcription factors C/EBP- α and PPAR- γ. In contrast, inhibition of Wnt signalling in pre-adipocytes results in spontaneous differentiation, indicating that preadipose cells produce endogenous Wnt that is a potent inhibitor of differentiation (Vertino et al., 2005). .
TGF- β is a cytokine that stimulates pre-adipocyte proliferation and inhibits adipogenesis in vitro. This is in agreement with the decreased adipose tissue development in mice overexpressing the gene encoding TGF-β. These inhibitory effects of TGF- β are mediated by the transcription factor SMAD3, which blocks the induction of C/EBP-α and PPAR-γ (Choy et al., 2000).
Although most fatty acids induce triacylglycerol storage in human fat cells, some fatty acids are known to block adipogenesis. Dietary medium-chain triglycerides decrease fat cell numbers and fat cell size in rodents, an effect that is likely to involve inhibition of adipose conversion and a decrease in PPAR- γ, C/EBP- α and SREBP-1c gene and protein expression (Brown and McKintosh, 2003).
Pre-adipocyte factor 1 (Pref-1) is a transmembrane protein that belongs to a family of epidermal-growth-factor-like repeats containing proteins. Pref-1 expression is high in pre-adipocytes and is strongly repressed upon adipogenesis.Constitutive Pref-1 expression inhibits adipose conversion. A soluble form of Pref-1 is sufficient to decrease adipose tissue mass and insulin sensitivity. In addition, Pref-1 mice are obese (Villena et al., 2002).
Measurement of fat distribution
Some adipose tissue is responsive to sex hormones, such as adipose tissue in the breasts and thighs, whereas other depots, such as fat on the neck and upper back, are more responsive to glucocorticoids—forming a so-called “buffalo-hump” in humans with an excess of glucocorticoids, such as in Cushing’s disease. The acquired form of lipodystrophy associated with treatment for HIV produces a similar kind of buffalo-hump. Fat distribution, even in thin individuals with steady body weight, changes with age, decreasing in retro-orbital fat and subcutaneous fat and increasing in intra-abdominal fat Striking differences in WAT distribution can also be observed in individuals with heritable forms of partial lipodystrophy (Agarwal and Garg, 2006) .
Fat distribution, is measured using either imaging or anthropometric techniques. Measurement has focused on assessment and differentiation of subcutaneous and intraabdominal (visceral) depots; however, measurement of fat residing in muscle has become of interest. Imaging techniques have the advantage of providing separate measurements of fat in these three different depots, but they remain too expensive for use in most clinical and community settings. Anthropometric measurements cannot provide a direct assessment of the amount of fat in different depots, but they can provide variables that correlate with assessments from imagining techniques and are quick, inexpensive, and noninvasive (Aronne and Segal, 2002).
Imaging techniques
Computed tomography (CT) and magnetic resonance imaging (MRI) are considered the most precise methods for measuring body fat distribution. MRI has the advantage of not exposing subjects to radiation. Dual energy X-ray is primarily used to measure bone mineral content and total body fat.This technique can measure total abdominal fat, but it cannot differentiate between visceral and subcutaneous fat (Stevens et al., 2001).
CT scans have shown that approximately 12% of fat in normal weight subjects is among and inside muscles. Some researchers advocate considering this fat in a separate compartment, which, from a metabolic standpoint, is more closely related to visceral fat. Some researchers have suggested that subcutaneous fat be separated into deep and superficial layers separated by the ‘fascia superficialis (Seidell et al., 2001).
Anthropometric techniques
Anthropometric indices used to measure fat patterning include skinfold thicknesses, circumferences, sagittal diameter, and ratios such as waist-to-hip, waist-to-thigh, waist-to-height, and subscapular-to-triceps skinfolds. Skinfold thickness and skinfold ratio have not been found to be very well correlated with metabolic measurements or with visceral fat and are not recommended for use as indicators of fat patterning (Molarius and Seidell, 1998).

Waist circumference (WC) alone and waist-to-hip ratio (WHR) are the most popular anthropometric methods used to measure fat distribution in both clinical and community settings. Both measures are correlated with visceral fat. Waist circumferences measured at four sites (immediately below the lowest rib, at the narrowest point, midpoint between the lowest rib and the iliac crest, and immediately above the iliac crest) have been compared and found to differ from each other. The highest correlations with risk factors were obtained when WHR was calculated as the waist measured at the point midway between the lower rib margin and iliac crest (approximately 1 inch above the umbilicus) or when the waist was measured at the umbilicus and hips measured at the widest point of the buttocks. Although two different waist measurements have been demonstrated to perform equally well, the bony landmark measurement (the point midway between the lower rib margin and iliac crest) may be preferred since the umbilicus may shift position when an individual gains or loses weight. The World Health Organization (WHO) has recommended measuring the waist at the midpoint between the lowest rib and the iliac crest, whereas immediately above the iliac crest is the site recommended by the National Institutes of Health (Wang et al., 2003).











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