Definition and Causes of Obesity − Rakyat Biologi

Obesity is not a single disorder. A variety of methods and criteria are used to diagnose the presence of obesity. It is the quantity of adipose tissue and not just total body weight that defines obesity. Several factors contribute to the development of obesity: genetics, environment, physiology, psychology, and undetermined.

Work from experimental animals shows clear genetic anomalies as one basic cause of obesity. Genes for obesity can be recessive, dominant, or polygenic. Recessive alleles that influence the development of obesity, including ob, db, and fa have been identified in various rodents (Table 1).

Table 1: Proposed location of chromosomal defect in several rodent models of obesity. All except one are autosomal recessive models. Inheritance in the yellow obese mouse is dominant.
Animal	Mutant Alleles	Proposed Chromosomal Locus
Hyperglycemic obese mouse	ob	6
Diabetic mouse	db	4
Yellow obese mouse.	Ay et al. at Agouti locus	2
Zucker obese rat	fa	5
Zucker brown Norway obese rat	fa	5
Wistar diabetic fatty rat	fa	5

In the human population, obesity is a feature of several recessive syndromes, including Bardet-Biedl, Lawrence-Moon, and Prader-Labhart-Willi, as well as, triglyceride storage diseases. These syndromes are relatively rare. A single genetic anomaly in the absence of other concurrent genetic syndromes has yet to be identified in humans. It is possible that alleles at particular loci exert a small effect that is not easily detectable by themselves. If these alleles exist at a large number of loci, collectively they may exert a substantial impact on obesity. Genes clearly influence body size and body fat distribution, and are likely to be involved in modulating human obesity.

In humans, it is difficult to separate genetic and environmental factors and assign the relative contribution of each to the development of obesity. Several familial, twin, and adoption studies have provided a means to study the contributions of heredity and environment. These studies provide strong suggestive data for a genetic component to obesity, as well as modulation of genes by environmental factors.

Environmental influences on obesity include food intake and degree of physical activity. Overeating relative to energy needs is a component of obesity development. However, from studies with experimental animals it is clear that many animals that develop obesity are energetically more efficient than lean animals; that is, for a given amount of food, the obesity-prone animals deposit more fat than do the obesity-resistant animals. In fact, when genetically obese rodents are not allowed to overeat from birth, they are still considerably fatter than their lean brothers and sisters.

The study of food intake in humans is confounded by the fact that some obese individuals under-report the amount of food they eat. The composition of the diet can also influence obesity. Overweight individuals have been shown to consume more high-fat foods than normal-weight individuals.

The amount of energy that an individual expends will also influence the development of obesity. Increased level of activity is associated with leanness. Other than the energy deficit that occurs with exercise, metabolic changes with training also impact fat utilization and storage. Trained individuals have an increased lipolytic capacity compared to sedentary persons. Both basal and catecholamine-stimulated lipolysis are higher in fat cells from trained individuals. In rats that are obesity-prone, prior to the onset of obesity, catecholamine-stimulated lipolysis is lower in their fat cells than in fat cells from obesity-resistant rats. An important benefit of exercise during weight loss is that it results in preservation of fat-free mass and allows fat loss that is equivalent to or greater than weight loss.

Several physiological factors may be involved in the development of obesity. These include altered adipose tissue metabolism, hormonal changes, and changes at sites in the brain that control satiety, particularly in the hypothalamus. There may be some kind of abnormal signal that affects adipose tissue metabolism and alters fuel partitioning, directing increased storage in adipose tissue instead of use in muscle. This abnormal signal has not been identified. However, lipoprotein lipase has been found to be increased in obesity, and this enzyme can increase the storage of triglycerides in adipose tissue. Hormonal changes that may affect obesity include hyperinsulinemia and changes in pituitary or adrenal function. Hormonal changes during pregnancy promote fat deposition. If weight gain is excessive, it can result in lifelong obesity.

The role of psychological variables in the development of obesity is difficult to define. There is no unifying theme. Some obese individuals have eating disorders. Other obese individuals may eat in response to stress or depression. Still other obese individuals may eat large meals or may eat rapidly. It has also been suggested that some obese individuals may be restrained eaters, and when there is a break in their usual routine, they respond by excessive eating.

Although a number of mechanisms have been identified for the development of obesities, the exact picture is far from clear. For many individuals, there may be an underlying biological defect. When this individual comes into contact with a plentiful, good-tasting, high-fat food in an environment that promotes inactivity, obesity results. Also important is the fact that while many people may lose weight, there is little success in keeping the weight off. The reasons for this recidivism and possible solutions are the focus of current research.