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"Adiposo" vuelve a dirigir aquí. Para la criatura ficticia de Doctor Who, consulte la Lista de criaturas y extraterrestres del universo de Doctor Who (0–9, A – G) § Adiposo .
Ver también: Grasa
Tejido adiposo
Illu connective tissues 1.jpg
El tejido adiposo es uno de los principales tipos de tejido conectivo .
Adipocyte types.jpg
Morfología de tres clases diferentes de adipocitos.
Pronunciación/ Æ d del ɪ ˌ p oʊ s / ( escuchar )About this sound
Identificadores
MallaD000273
FMA20110
Terminología anatómica

El tejido adiposo , la grasa corporal o simplemente la grasa es un tejido conectivo laxo compuesto principalmente por adipocitos . [1] Además de los adipocitos, el tejido adiposo contiene la fracción vascular estromal (FVS) de células que incluyen preadipocitos , fibroblastos , células endoteliales vasculares y una variedad de células inmunes como los macrófagos del tejido adiposo . El tejido adiposo se deriva de los preadipocitos. Su función principal es almacenar energía en forma de lípidos , aunque también amortigua y aíslael cuerpo. Lejos de ser hormonalmente inerte, el tejido adiposo ha sido reconocido en los últimos años como un órgano endocrino importante , [2] ya que produce hormonas como leptina , estrógeno , resistina y citocina (especialmente TNFα ). Los dos tipos de tejido adiposo son el tejido adiposo blanco (WAT), que almacena energía, y el tejido adiposo marrón (BAT), que genera calor corporal. La formación de tejido adiposo parece estar controlada en parte por el gen adiposo . El tejido adiposo, más específicamente el tejido adiposo marrón, fue identificado por primera vez por el naturalista suizo.Conrad Gessner en 1551. [3]

Características anatómicas [ editar ]

Distribución de la grasa blanca en el cuerpo humano.

En los seres humanos, el tejido adiposo se localiza: debajo de la piel ( grasa subcutánea ), alrededor de los órganos internos ( grasa visceral ), en la médula ósea ( médula ósea amarilla ), intermuscular ( sistema muscular ) y en la mama ( tejido mamario ). El tejido adiposo se encuentra en lugares específicos, que se conocen como depósitos adiposos . Aparte de los adipocitos, que comprenden el porcentaje más alto de células dentro del tejido adiposo, están presentes otros tipos de células, denominados colectivamente fracción vascular estromal (FVS) de células. La FVS incluye preadipocitos , fibroblastos , macrófagos del tejido adiposoy células endoteliales .

El tejido adiposo contiene muchos vasos sanguíneos pequeños . En el sistema tegumentario , que incluye la piel, se acumula en el nivel más profundo, la capa subcutánea , proporcionando aislamiento del calor y del frío. Alrededor de los órganos, proporciona un acolchado protector. Sin embargo, su función principal es ser una reserva de lípidos, que pueden oxidarse para satisfacer las necesidades energéticas del cuerpo y protegerlo del exceso de glucosa al almacenar los triglicéridos producidos por el hígado a partir de los azúcares, aunque algunas evidencias sugieren que la mayoría de la síntesis de lípidos de los carbohidratos se produce en el propio tejido adiposo. [4]Los depósitos adiposos en diferentes partes del cuerpo tienen diferentes perfiles bioquímicos. En condiciones normales, proporciona al cerebro información sobre el hambre y la dieta.

Ratones [ editar ]

El ratón obeso de la izquierda tiene grandes reservas de tejido adiposo. No puede producir la hormona leptina . Esto hace que el ratón tenga hambre y coma más, lo que resulta en obesidad. A modo de comparación, a la derecha se muestra un ratón con una cantidad normal de tejido adiposo.

Los ratones tienen ocho depósitos adiposos principales, cuatro de los cuales se encuentran dentro de la cavidad abdominal . [1] Los depósitos gonadales emparejados se adhieren al útero y los ovarios en las mujeres y al epidídimo y los testículos en los hombres; los depósitos retroperitoneales emparejados se encuentran a lo largo de la pared dorsal del abdomen , rodeando el riñón y, cuando son masivos, se extienden hacia la pelvis. El depósito mesentérico forma una red similar a un pegamento que sostiene los intestinos y el depósito omental (que se origina cerca del estómago y el bazo).) y, cuando es masivo, se extiende hacia el abdomen ventral. Tanto el depósito mesentérico como el omental incorporan mucho tejido linfoide como ganglios linfáticos y manchas lechosas , respectivamente.

Los dos depósitos superficiales son los depósitos inguinales emparejados, que se encuentran anterior al segmento superior de las extremidades traseras (debajo de la piel) y los depósitos subescapulares, mezclas mediales emparejadas de tejido adiposo marrón adyacentes a regiones de tejido adiposo blanco, que se encuentran debajo de la piel entre las crestas dorsales de las escápulas. La capa de tejido adiposo marrón en este depósito suele estar cubierta por un "glaseado" de tejido adiposo blanco; a veces, estos dos tipos de grasa (marrón y blanca) son difíciles de distinguir. Los depósitos inguinales encierran el grupo inguinal de ganglios linfáticos. Los depósitos menores incluyen el pericárdico , que rodea el corazón, y los depósitos poplíteos emparejados, entre los músculos principales detrás de las rodillas, cada uno de los cuales contiene un ganglio linfático grande .[5] De todos los depósitos en el ratón, los depósitos gonadales son los más grandes y los más fácilesde disecar, [6] que comprenden aproximadamente el 30% de la grasa diseccionable. [7]

Obesidad [ editar ]

En una persona obesa , el exceso de tejido adiposo que cuelga hacia abajo del abdomen se denomina panículo . Un panículo complica la cirugía del individuo con obesidad mórbida. Puede permanecer literalmente como un "delantal de piel" si una persona con obesidad severa pierde rápidamente grandes cantidades de grasa (un resultado común de la cirugía de bypass gástrico ). La obesidad se trata con ejercicio, dieta y terapia conductual. La cirugía reconstructiva es un método de tratamiento. [8]

Grasa visceral[ editar ]

Obesidad abdominal en hombres ("barriga cervecera")
Ver también: obesidad abdominal

La grasa visceral o grasa abdominal [9] (también conocida como grasa de órganos o grasa intraabdominal) se encuentra dentro de la cavidad abdominal , empaquetada entre los órganos (estómago, hígado, intestinos, riñones, etc.). La grasa visceral es diferente de la grasa subcutánea debajo de la piel y la grasa intramuscular intercalada en los músculos esqueléticos . La grasa en la parte inferior del cuerpo, como en los muslos y las nalgas, es subcutánea y no es un tejido espaciado uniformemente, mientras que la grasa en el abdomen es principalmente visceral y semifluida. [10] La grasa visceral se compone de varios depósitos adiposos, que incluyen mesentérico , epidídimo tejido adiposo blanco (EWAT) y depósitos perirrenal . La grasa visceral a menudo se expresa en términos de su área en cm 2 (VFA, área de grasa visceral). [11]

Un exceso de grasa visceral se conoce como obesidad central , o "grasa abdominal", en la que el abdomen sobresale excesivamente. Los nuevos desarrollos, como el Índice de volumen corporal (BVI), están diseñados específicamente para medir el volumen abdominal y la grasa abdominal. El exceso de grasa visceral también está vinculada a la diabetes tipo 2 , [12] resistencia a la insulina , [13] enfermedades inflamatorias , [14] y otras enfermedades relacionada con la obesidad. [15] Asimismo, se ha demostrado que la acumulación de grasa en el cuello (o tejido adiposo cervical) está asociada con la mortalidad. [16] Varios estudios han sugerido que la grasa visceral se puede predecir a partir de medidas antropométricas simples,[17] y predice la mortalidad con mayor precisión que el índice de masa corporal o la circunferencia de la cintura. [18]

Los hombres tienen más probabilidades de tener grasa almacenada en el abdomen debido a las diferencias de hormonas sexuales . La hormona sexual femenina hace que la grasa se almacene en las nalgas, los muslos y las caderas de las mujeres. [19] [20] Cuando las mujeres llegan a la menopausia y el estrógeno producido por los ovarios disminuye, la grasa migra desde las nalgas, las caderas y los muslos hasta la cintura; [21] Posteriormente, la grasa se almacena en el abdomen. [10]

El ejercicio de alta intensidad es una forma de reducir eficazmente la grasa abdominal total. [22] [23] Un estudio sugiere que se requieren al menos 10 MET- horas por semana de ejercicio aeróbico para reducir la grasa visceral. [24] Una dieta restringida en energía combinada con ejercicio reducirá la grasa corporal total y la proporción de tejido adiposo visceral a tejido adiposo subcutáneo, lo que sugiere una movilización preferencial de la grasa visceral sobre la grasa subcutánea. [25]

Grasa epicárdica [ editar ]

El tejido adiposo epicárdico (EAT) es una forma particular de grasa visceral que se deposita alrededor del corazón y se encuentra como un órgano metabólicamente activo que genera varias moléculas bioactivas, que podrían afectar significativamente la función cardíaca . [26] Se han observado diferencias marcadas en los componentes al comparar el EAT con la grasa subcutánea , lo que sugiere un impacto específico de depósito de los ácidos grasos almacenados en la función y el metabolismo de los adipocitos. [27]

Grasa subcutánea [ editar ]

Ver también: porcentaje de grasa corporal
Microanatomía de la grasa subcutánea

La mayor parte de la grasa no visceral restante se encuentra justo debajo de la piel en una región llamada hipodermis . [28] Esta grasa subcutánea no está relacionada con muchas de las patologías clásicas relacionadas con la obesidad, como las enfermedades cardíacas , el cáncer y los accidentes cerebrovasculares , y algunas pruebas incluso sugieren que podría ser protectora. [29] El patrón típicamente femenino (o ginecoide) de distribución de la grasa corporal alrededor de las caderas, muslos y glúteos es la grasa subcutánea y, por lo tanto, representa un riesgo menor para la salud en comparación con la grasa visceral. [30] [31]

Como todos los demás órganos grasos, la grasa subcutánea es una parte activa del sistema endocrino, que secreta las hormonas leptina y resistina . [28]

La relación entre la capa adiposa subcutánea y la grasa corporal total en una persona a menudo se modela mediante ecuaciones de regresión. La más popular de estas ecuaciones fue formada por Durnin y Wormersley, quienes probaron rigurosamente muchos tipos de pliegues cutáneos y, como resultado, crearon dos fórmulas para calcular la densidad corporal de hombres y mujeres. Estas ecuaciones presentan una correlación inversa entre los pliegues cutáneos y la densidad corporal: a medida que aumenta la suma de los pliegues cutáneos, la densidad corporal disminuye. [32]

Factores como el sexo, la edad, el tamaño de la población u otras variables pueden hacer que las ecuaciones sean inválidas e inutilizables y, a partir de 2012 , las ecuaciones de Durnin y Wormersley siguen siendo solo estimaciones del verdadero nivel de gordura de una persona. Todavía se están creando nuevas fórmulas. [32]

Grasa de médula [ editar ]

La grasa de la médula ósea, también conocida como tejido adiposo de la médula ósea ( MAT ), es un depósito adiposo poco conocido que reside en el hueso y está intercalado con células hematopoyéticas y elementos óseos. Los adipocitos en este depósito se derivan de células madre mesenquimales (MSC) que pueden dar lugar a células grasas, células óseas y otros tipos de células. El hecho de que MAT aumenta en el contexto de restricción calórica / anorexia es una característica que distingue a este depósito de otros depósitos de grasa. [33] [34] [35] El ejercicio regula MAT, disminuyendo la cantidad de MAT y disminuyendo el tamaño de los adipocitos de la médula. [36] [37] [38] La regulación del ejercicio de la grasa de la médula ósea sugiere que tiene cierta similitud fisiológica con otros depósitos de grasa blanca. Además, el aumento de MAT en la obesidad sugiere una similitud con los depósitos de grasa blanca. [36]

Grasa ectópica [ editar ]

La grasa ectópica es el almacenamiento de triglicéridos en tejidos distintos del tejido adiposo, que se supone que contienen solo pequeñas cantidades de grasa, como el hígado , el músculo esquelético , el corazón y el páncreas . [1] Esto puede interferir con las funciones celulares y, por lo tanto, la función de los órganos y se asocia con la resistencia a la insulina en la diabetes tipo 2. [39] Se almacena en cantidades relativamente altas alrededor de los órganos de la cavidad abdominal , pero no debe confundirse con la grasa visceral.

Se desconoce la causa específica de la acumulación de grasa ectópica. Es probable que la causa sea una combinación de factores genéticos, ambientales y de comportamiento que están involucrados en la ingesta excesiva de energía y la disminución de la actividad física. Una pérdida de peso sustancial puede reducir las reservas de grasa ectópica en todos los órganos y esto se asocia con una mejora de la función de ese órgano. [39]

En el último caso, las intervenciones de pérdida de peso no invasivas como la dieta o el ejercicio pueden disminuir la grasa ectópica (particularmente en el corazón y el hígado) en niños y adultos con sobrepeso u obesidad. [40] [41]

Fisiología [ editar ]

Free fatty acids (FFAs) are liberated from lipoproteins by lipoprotein lipase (LPL) and enter the adipocyte, where they are reassembled into triglycerides by esterifying them onto glycerol. Human fat tissue contains about 87% lipids.[42]

There is a constant flux of FFAs entering and leaving adipose tissue. The net direction of this flux is controlled by insulin and leptin—if insulin is elevated, then there is a net inward flux of FFA, and only when insulin is low can FFA leave adipose tissue. Insulin secretion is stimulated by high blood sugar, which results from consuming carbohydrates.[43]

En los seres humanos, la lipólisis (hidrólisis de triglicéridos en ácidos grasos libres) se controla mediante el control equilibrado de los receptores adrenérgicos B lipolíticos y la antilipólisis mediada por el receptor adrenérgico a2A.

Las células grasas tienen un papel fisiológico importante en el mantenimiento de los niveles de triglicéridos y ácidos grasos libres, así como en la determinación de la resistencia a la insulina . La grasa abdominal tiene un perfil metabólico diferente , siendo más propensa a inducir resistencia a la insulina. Esto explica en gran medida por qué la obesidad central es un marcador de intolerancia a la glucosa y es un factor de riesgo independiente de enfermedad cardiovascular (incluso en ausencia de diabetes mellitus e hipertensión ). [44] Los estudios de monos hembras en la Universidad de Wake Forest (2009) descubrieron que los individuos que sufren de mayorestrés tienen niveles más altos de grasa visceral en sus cuerpos. Esto sugiere un posible vínculo de causa y efecto entre los dos, en el que el estrés promueve la acumulación de grasa visceral, que a su vez provoca cambios hormonales y metabólicos que contribuyen a las enfermedades cardíacas y otros problemas de salud. [45]

Los recientes avances en biotecnología han permitido la recolección de células madre adultas del tejido adiposo, lo que permite la estimulación del recrecimiento del tejido utilizando las propias células del paciente. Además, según se informa, las células madre derivadas de tejido adiposo tanto de humanos como de animales pueden reprogramarse eficazmente en células madre pluripotentes inducidas sin la necesidad de células alimentadoras . [46] El uso de células del propio paciente reduce la posibilidad de rechazo de tejido y evita problemas éticos asociados con el uso de células madre embrionarias humanas . [47] Un creciente cuerpo de evidencia también sugiere que diferentes depósitos de grasa (es decir, abdominal, omental, pericárdico) producen células madre derivadas de tejido adiposo con diferentes características.[47] [48] Estas características dependientes del depósito incluyen la tasa de proliferación , el inmunofenotipo , el potencial de diferenciación , la expresión génica y la sensibilidad a las condiciones de cultivo hipóxicas. [49] Los niveles de oxígeno parecen jugar un papel importante en el metabolismo y, en general, en la función de las células madre derivadas de tejido adiposo. [50]

El tejido adiposo es una fuente periférica importante de aromatasa tanto en hombres como en mujeres, lo que contribuye a la producción de estradiol . [51]

Las hormonas derivadas del tejido adiposo incluyen:

  • Adiponectina
  • Resistir
  • Inhibidor del activador del plasminógeno-1 (PAI-1)
  • TNFα
  • IL-6
  • Leptina
  • Estradiol (E2)

Los tejidos adiposos también secretan un tipo de citocinas (proteínas de señalización de célula a célula) llamadas adipocinas (citocinas adiposas), que desempeñan un papel en las complicaciones asociadas a la obesidad. El tejido adiposo perivascular libera adipocinas como la adiponectina que afectan la función contráctil de los vasos que rodean. [1] [52]

Grasa parda [ editar ]

Célula de grasa marrón
Artículo principal: tejido adiposo marrón

Brown fat or brown adipose tissue (BAT) is a specialized form of adipose tissue important for adaptive thermogenesis in humans and other mammals. BAT can generate heat by "uncoupling" the respiratory chain of oxidative phosphorylation within mitochondria through tissue-specific expression of uncoupling protein 1 (UCP1).[53] BAT is primarily located around the neck and large blood vessels of the thorax, where it may effectively act in heat exchange. BAT is robustly activated upon cold exposure by the release of catecholamines from sympathetic nerves that results in UCP1 activation. BAT activation may also occur in response to overfeeding.[54] UCP1 activity is stimulated by long chain fatty acids that are produced subsequent to β-adrenergic receptor activation.[53] UCP1 is proposed to function as a fatty acid proton symporter, although the exact mechanism has yet to be elucidated.[55] In contrast, UCP1 is inhibited by ATP, ADP, and GTP.[56]

Attempts to simulate this process pharmacologically have so far been unsuccessful. Techniques to manipulate the differentiation of "brown fat" could become a mechanism for weight loss therapy in the future, encouraging the growth of tissue with this specialized metabolism without inducing it in other organs. A review on the eventual therapeutic targeting of brown fat to treat human obesity was published by Samuelson and Vidal-Puig in 2020.[57]

Until recently, brown adipose tissue was thought to be primarily limited to infants in humans, but new evidence has now overturned that belief. Metabolically active tissue with temperature responses similar to brown adipose was first reported in the neck and trunk of some human adults in 2007,[58] and the presence of brown adipose in human adults was later verified histologically in the same anatomical regions.[59][60][61]

Beige fat and WAT browning[edit]

Browning of WAT, also referred to as "beiging", occurs when adipocytes within WAT depots develop features of BAT. Beige adipocytes take on a multilocular appearance (containing several lipid droplets) and increase expression of uncoupling protein 1 (UCP1).[62] In doing so, these normally energy-storing adipocytes become energy-releasing adipocytes.

The calorie-burning capacity of brown and beige fat has been extensively studied as research efforts focus on therapies targeted to treat obesity and diabetes. The drug 2,4-dinitrophenol, which also acts as a chemical uncoupler similarly to UCP1, was used for weight loss in the 1930s. However, it was quickly discontinued when excessive dosing led to adverse side effects including hyperthermia and death.[62] β3 agonists, like CL316,243, have also been developed and tested in humans. However, the use of such drugs has proven largely unsuccessful due to several challenges, including varying species receptor specificity and poor oral bioavailability.[63]

Cold is a primary regulator of BAT processes and induces WAT browning. Browning in response to chronic cold exposure has been well documented and is a reversible process. A study in mice demonstrated that cold-induced browning can be completely reversed in 21 days, with measurable decreases in UCP1 seen within a 24-hour period.[64] A study by Rosenwald et al. revealed that when the animals are re-exposed to a cold environment, the same adipocytes will adopt a beige phenotype, suggesting that beige adipocytes are retained.[65]

Transcriptional regulators, as well as a growing number of other factors, regulate the induction of beige fat. Four regulators of transcription are central to WAT browning and serve as targets for many of the molecules known to influence this process.[66] These include peroxisome proliferator-activated receptor gamma (PPARγ), PR domain containing 16 (PRDM16),[67] peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), and Early B-Cell Factor-2 (EBF2).[68][69][70]

The list of molecules that influence browning has grown in direct proportion to the popularity of this topic and is constantly evolving as more knowledge is acquired. Among these molecules are irisin and fibroblast growth factor 21 (FGF21), which have been well-studied and are believed to be important regulators of browning. Irisin is secreted from muscle in response to exercise and has been shown to increase browning by acting on beige preadipocytes.[71] FGF21, a hormone secreted mainly by the liver, has garnered a great deal of interest after being identified as a potent stimulator of glucose uptake and a browning regulator through its effects on PGC-1α.[62] It is increased in BAT during cold exposure and is thought to aid in resistance to diet-induced obesity[72] FGF21 may also be secreted in response to exercise and a low protein diet, although the latter has not been thoroughly investigated.[73][74] Data from these studies suggest that environmental factors like diet and exercise may be important mediators of browning. In mice, it was found that beiging can occur through the production of methionine-enkephalin peptides by type 2 innate lymphoid cells in response to interleukin 33.[75]

Genomics and bioinformatics tools to study browning[edit]

Due to the complex nature of adipose tissue and a growing list of browning regulatory molecules, great potential exists for the use of bioinformatics tools to improve study within this field. Studies of WAT browning have greatly benefited from advances in these techniques, as beige fat is rapidly gaining popularity as a therapeutic target for the treatment of obesity and diabetes.

DNA microarray is a bioinformatics tool used to quantify expression levels of various genes simultaneously, and has been used extensively in the study of adipose tissue. One such study used microarray analysis in conjunction with Ingenuity IPA software to look at changes in WAT and BAT gene expression when mice were exposed to temperatures of 28 and 6 °C.[76] The most significantly up- and downregulated genes were then identified and used for analysis of differentially expressed pathways. It was discovered that many of the pathways upregulated in WAT after cold exposure are also highly expressed in BAT, such as oxidative phosphorylation, fatty acid metabolism, and pyruvate metabolism.[76] This suggests that some of the adipocytes switched to a beige phenotype at 6 °C. Mössenböck et al. also used microarray analysis to demonstrate that insulin deficiency inhibits the differentiation of beige adipocytes but does not disturb their capacity for browning.[77] These two studies demonstrate the potential for the use of microarray in the study of WAT browning.

RNA sequencing (RNA-Seq) is a powerful computational tool that allows for the quantification of RNA expression for all genes within a sample. Incorporating RNA-Seq into browning studies is of great value, as it offers better specificity, sensitivity, and a more comprehensive overview of gene expression than other methods. RNA-Seq has been used in both human and mouse studies in an attempt characterize beige adipocytes according to their gene expression profiles and to identify potential therapeutic molecules that may induce the beige phenotype. One such study used RNA-Seq to compare gene expression profiles of WAT from wild-type (WT) mice and those overexpressing Early B-Cell Factor-2 (EBF2). WAT from the transgenic animals exhibited a brown fat gene program and had decreased WAT specific gene expression compared to the WT mice.[78] Thus, EBF2 has been identified as a potential therapeutic molecule to induce beiging.

Chromatin immunoprecipitation with sequencing (ChIP-seq) is a method used to identify protein binding sites on DNA and assess histone modifications. This tool has enabled examination of epigenetic regulation of browning and helps elucidate the mechanisms by which protein-DNA interactions stimulate the differentiation of beige adipocytes. Studies observing the chromatin landscapes of beige adipocytes have found that adipogenesis of these cells results from the formation of cell specific chromatin landscapes, which regulate the transcriptional program and, ultimately, control differentiation. Using ChIP-seq in conjunction with other tools, recent studies have identified over 30 transcriptional and epigenetic factors that influence beige adipocyte development.[78]

Genetics[edit]

Main article: Genetics of obesity § Genes

The thrifty gene hypothesis (also called the famine hypothesis) states that in some populations the body would be more efficient at retaining fat in times of plenty, thereby endowing greater resistance to starvation in times of food scarcity. This hypothesis, originally advanced in the context of glucose metabolism and insulin resistance, has been discredited by physical anthropologists, physiologists, and the original proponent of the idea himself with respect to that context, although according to its developer it remains "as viable as when [it was] first advanced" in other contexts.[79][80]

In 1995, Jeffrey Friedman, in his residency at the Rockefeller University, together with Rudolph Leibel, Douglas Coleman et al. discovered the protein leptin that the genetically obese mouse lacked.[81][82][83] Leptin is produced in the white adipose tissue and signals to the hypothalamus. When leptin levels drop, the body interprets this as a loss of energy, and hunger increases. Mice lacking this protein eat until they are four times their normal size.

Leptin, however, plays a different role in diet-induced obesity in rodents and humans. Because adipocytes produce leptin, leptin levels are elevated in the obese. However, hunger remains, and—when leptin levels drop due to weight loss—hunger increases. The drop of leptin is better viewed as a starvation signal than the rise of leptin as a satiety signal.[84] However, elevated leptin in obesity is known as leptin resistance. The changes that occur in the hypothalamus to result in leptin resistance in obesity are currently the focus of obesity research.[85]

Gene defects in the leptin gene (ob) are rare in human obesity.[86] As of July 2010, only 14 individuals from five families have been identified worldwide who carry a mutated ob gene (one of which was the first ever identified cause of genetic obesity in humans)—two families of Pakistani origin living in the UK, one family living in Turkey, one in Egypt, and one in Austria[87][88][89][90][91]—and two other families have been found that carry a mutated ob receptor.[92][93] Others have been identified as genetically partially deficient in leptin, and, in these individuals, leptin levels on the low end of the normal range can predict obesity.[94]

Several mutations of genes involving the melanocortins (used in brain signaling associated with appetite) and their receptors have also been identified as causing obesity in a larger portion of the population than leptin mutations.[95]

Physical properties[edit]

Adipose tissue has a density of ~0.9 g/ml.[96] Thus, a person with more adipose tissue will float more easily than a person of the same weight with more muscular tissue, since muscular tissue has a density of 1.06 g/ml.[97]

Body fat meter[edit]

See also: Bioelectrical impedance analysis

A body fat meter is a widely available tool used to measure the percentage of fat in the human body. Different meters use various methods to determine the body fat to weight ratio. They tend to under-read body fat percentage.

In contrast with clinical tools, one relatively inexpensive type of body fat meter uses the principle of bioelectrical impedance analysis (BIA) in order to determine an individual's body fat percentage. To achieve this, the meter passes a small, harmless, electric current through the body and measures the resistance, then uses information on the person's weight, height, age, and sex to calculate an approximate value for the person's body fat percentage. The calculation measures the total volume of water in the body (lean tissue and muscle contain a higher percentage of water than fat), and estimates the percentage of fat based on this information. The result can fluctuate several percentage points depending on what has been eaten and how much water has been drunk before the analysis. Before bioelectrical impedance analysis machines were developed, there were many different ways in analyzing body composition such as skin fold methods using calipers, underwater weighing, whole body air displacement plethysmography (ADP) and DXA.

Animal studies[edit]

Within the fat (adipose) tissue of CCR2 deficient mice, there is an increased number of eosinophils, greater alternative Macrophage activation, and a propensity towards type 2 cytokine expression. Furthermore, this effect was exaggerated when the mice became obese from a high fat diet.[98]

Gallery[edit]

  • Diagrammatic sectional view of the skin (magnified).

  • White adipose tissue in paraffin section

  • Electronic instrument of body fat meter

See also[edit]

  • Adipose differentiation-related protein
  • Adiposopathy
  • Apelin
  • Bioelectrical impedance analysis – a method to measure body fat percentage.
  • Blubber – an extra thick form of adipose tissue found in some marine mammals.
  • Body fat percentage
  • Cellulite
  • Lipolysis
  • Lipodystrophy
  • Human fat used as pharmaceutical in traditional medicine
  • Obesity
  • Starvation
  • Steatosis (also called fatty change, fatty degeneration or adipose degeneration)
  • Stem cells
  • Subcutaneous fat
  • Bariatrics
  • Classification of obesity
  • Classification of childhood obesity
  • EPODE International Network, the world's largest obesity-prevention network
  • World Fit A program of the United States Olympic Committee (USOC), and the United States Olympians and Paralympians Association (USOP)
  • Obesity and walking
  • Social stigma of obesity

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Further reading[edit]

  • MeSH A10.165.114
  • Stock MJ, Cinti S (2003). "Adipose Tissue / Structure and Function of Brown Adipose Tissue". Encyclopedia of Food Sciences and Nutrition. pp. 29–34. doi:10.1016/B0-12-227055-X/00008-0. ISBN 978-0-12-227055-0.
  • Vernon RG, Flint DJ (2003). "Adipose Tissue / Structure and Function of White Adipose Tissue". Encyclopedia of Food Sciences and Nutrition. pp. 23–29. doi:10.1016/B0-12-227055-X/00007-9. ISBN 978-0-12-227055-0.

External links[edit]

  • Adipose tissue photomicrographs