Obesity continues to be a global pandemic. According to the World Health Organization, in 2016, more than 1.9 billion adults were overweight and 650 million had obesity (body mass index [BMI] > 30). Obesity has been linked to increased risk for type 2 diabetes, cardiovascular disease (CVD), mobility issues, and certain types of cancer (eg, adenocarcinoma of the esophagus, postmenopausal breast, colon, rectum). Unbalanced energy intake is a root cause of obesity, with underlying factors of genetic, environmental, socioeconomic, psychological, and behavioral etiology. Morphologic fat distribution varies in obesity. Here we discuss different types of obesity and adipose tissue, how disruption to hunger pathways affects energy balance, and factors that influence obesity.
Central Obesity
Central obesity, also referred to as visceral or abdominal obesity, is an accumulation of excess fat around the abdominal area. This type of obesity is associated with a higher risk for health issues, particularly type 2 diabetes and CVD. Central obesity is more common in men than women and can be caused by a multitude of factors, specifically hormonal imbalance (eg, hypercortisolism seen in Cushing syndrome), along with stress and poor lifestyle choices. Central weight distribution is particularly concerning because the fat accumulates around internal organs and is metabolically active, increasing the risk for insulin resistance and other sequelae seen in metabolic syndrome.
Gynoid Obesity
Also known as pear-shaped obesity, gynoid obesity describes the accumulation of fat around the hips, thighs, and buttocks. As the name suggests, gynoid obesity is more common in women. In gynoid obesity, certain genetic and hormonal factors affect the distribution of fat. Although gynoid obesity is associated with a lower risk of developing CVD and other diseases compared with other obesity types, it can still be a risk factor for inflammatory conditions and atherosclerosis.
Android Obesity
In android obesity, also referred to as apple-shaped obesity, fat tends to accumulate in the upper body, specifically around the abdomen, chest area, and upper limbs. Android obesity can be confused with central obesity because these types have similar epidemiologic and risk-factor profiles, including their increased prevalence in men and increased risk of developing type 2 diabetes and CVD.
Sarcopenic Obesity
Sarcopenic obesity, characterized by low muscle mass and high body fat, typically occurs in older people. Studies have shown an accelerated loss of muscle mass with age and worsening insulin resistance, leading to increased body fat. It is also associated with increased CVD-associated mortality and all-cause mortality. The loss of muscle mass in sarcopenic obesity also decreases mobility and increases the risk for falls and fractures.
Assessing Abdominal Adiposity to Determine Obesity Type
Obesity type can be determined by measuring waist circumference, a simple and underutilized tool. Per National Institutes of Health criteria, a waist circumference > 35 in for women and > 40 in for men is generally suggestive of central obesity. Waist circumference measurements should be used in conjunction with the person's BMI and body fat percentage. Muscle, water, and fat composition of the body can be determined using either a dual-energy x-ray absorptiometry or bioelectrical impedance analysis. According to the World Health Organization criteria, central obesity is defined by a waist circumference ≥ 94 cm for men and ≥ 80 cm for women.
Adipose Tissue Type: WAT and BAT
Each of the two main types of fat in adipose tissue, white adipose fat (WAT) and brown adipose tissue (BAT), has a distinct morphology and function. WAT, the most abundant type in adults, provides insulation and stores energy as triglycerides. Under a microscope, WAT may appear as one fat droplet "pushing" all cell contents to the periphery. In contrast, BAT appears as multiple, smaller fat droplets within one cell. Unlike WAT, BAT is metabolically active and thermogenic, which is why it is mostly concentrated in the torso region. In newborns, BAT comprises approximately 5% of body mass, but as humans age, they accumulate more WAT. In addition to WAT and BAT, beige fat cells are present in white adipose tissue and perform functions similar to WAT and BAT. In fact, beige fat cells act more like WAT; however, when exposed to cold temperatures, they function like BAT and dissipate heat. As a person develops obesity and ages over time, WAT content increases while BAT and beige content declines, a process called "whitening." Much research is underway to better elucidate implications in obesity.
Fat cells increase rapidly during late childhood, puberty, and, to some extent, adulthood. BAT activity increases during puberty and adolescent years, corresponding to lower adiposity and body weight gain. Accumulation of adipose tissue in adulthood (eg, aging, pregnancy), hypertrophic obesity, usually correlates with an increase in the size of fat cells vs an increase in the number of cells.
Hunger Pathways and Energy Balance
Several internal pathways throughout the central nervous system and peripheral pathways control energy expenditure. In the brain, the two main pathways that govern hunger are the homeostatic and the hedonic pathways. The homeostatic pathway (ie, the biological hunger pathway) controls energy balance by signaling metabolic hunger, whereas the hedonic pathway is directly related to the feeling of enjoyment and reward associated with eating. When the hedonic pathway overrides the homeostatic pathway, it can trigger food consumption even in the absence of hunger (eg, episodes of stress overeating) which can lead to obesity. Hypothalamic obesity results from injury to the hypothalamus through strokes, trauma, or other disease processes, and is characterized by malfunction of energy balance and homeostasis.
On the peripheral side, several hormones govern the degree of hunger and satiety. Because most gut hormones (eg, glucagon-like peptide 1, peptide YY, cholecystokinin) are related to satiety, they are secreted when food is ingested. Novel obesity drugs, such as semaglutide 2.4 mg and upcoming tirzepatide 15 mg, exert their effects via these gut hormone analogues. Ghrelin, the only known hunger hormone, is secreted at the fundus of the stomach in response to energy deficiency. Directly antithetical to ghrelin is leptin, the hormone secreted by the fat cells and responsible for signaling satiety. There is also evidence that gut microbiota are responsible for energy regulation as well as signaling of hunger and satiety. In adults with obesity, there is a degree of leptin resistance, which attenuates the effect of leptin to signal satiety. Further research into the safety and effectiveness of medications for weight loss is needed.
Factors That Influence Obesity
Although the etiology of most forms of obesity is influenced by genetics, behavioral patterns, and socioeconomic status, other external factors can influence the homeostatic and hedonic pathways. Certain medications (eg, steroids and some antipsychotic, antidepressant, and antiretroviral drugs) can disrupt the energy balance in the body and cause central obesity. Moreover, endocrine disorders such as Cushing disease, type 2 diabetes, and growth-hormone deficiencies predispose people to obesity. Certain genetic mutations and syndromes can also cause increased eating and obesity, namely MCR4 mutations, leptin receptor mutations, chromosomal abnormalities (eg, Prader-Willi Syndrome), and childhood genetic disorders (eg, Bardet-Biedl Syndrome). Each of these conditions can cause early-childhood-onset and rapid obesity and may be associated with a family history and the presence of intellectual difficulties. Therefore, the development of obesity is not attributable to the individual person but rather to a multitude of complex, interplaying factors that influence the central energy circuitry of the brain.
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Cite this: Metabolic Complications of Obesity: What Role Does Body Fat Distribution Play? - Medscape - Sep 15, 2023.
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