Page 317 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster

Nutritional Diseases 303

Table 7–10 Selected Trace Elements and Deficiency Syndromes

Element Function Basis of Deficiency Clinical Features
Zinc Component of enzymes, principally oxidases Rash around eyes, mouth, nose, and anus
Inadequate supplementation in artificial
diets called acrodermatitis enteropathica
Anorexia and diarrhea
Interference with absorption by other Growth retardation in children
dietary constituents Depressed mental function
Depressed wound healing and immune
Inborn error of metabolism
response
Iron Essential component of hemoglobin as well Inadequate diet Impaired night vision
Iodine as several iron-containing metalloenzymes Chronic blood loss Infertility
Copper Inadequate supply in food and water Hypochromic, microcytic anemia
Component of thyroid hormone Inadequate supplementation in artificial diet
Fluoride Component of cytochrome c oxidase, Interference with absorption Goiter and hypothyroidism
Selenium Muscle weakness
dopamine β-hydroxylase, tyrosinase, lysyl Inadequate supply in soil and water Neurologic defects
oxidase, and unknown enzyme involved in Inadequate supplementation Abnormal collagen cross-linking
cross-linking collagen Inadequate amounts in soil and water
Mechanism unknown Dental caries

Component of glutathione peroxidase Myopathy
Antioxidant with vitamin E Cardiomyopathy (Keshan disease)

India. Globally, the World Health Organization (WHO) The etiology of obesity is complex and incompletely
estimates that by 2015, 700 million adults will be obese. The understood. Involved are genetic, environmental, and psy-
causes of this epidemic are complex but undoubtedly are chologic factors. However, simply put, obesity is a disorder
related to societal changes in diet and levels of physical of energy balance. The two sides of the energy equation,
activity. Obesity is associated with an increased risk of several intake and expenditure, are finely regulated by neural and
important diseases (e.g., diabetes, hypertension), making it a hormonal mechanisms, so that body weight is maintained
major public health concern. Indeed, in 2009 it was esti- within a narrow range for many years. Apparently, this
mated that the health care cost of obesity had risen to $147 fine balance is controlled by an internal set point, or “lipo-
billion annually in the United States, a price tag that stat,” that senses the quantity of energy stores (adipose
appears bound to rise as the nation’s collective waistline tissue) and appropriately regulates food intake as well as
expands. energy expenditure. In recent years, several “obesity genes”
have been identified. As might be expected, they encode
Obesity is defined as a state of increased body weight, the molecular components of the physiologic system that
due to adipose tissue accumulation, that is of sufficient regulates energy balance. A key player in energy homeo-
magnitude to produce adverse health effects. How does stasis is the LEP gene and its product, leptin. This unique
one measure fat accumulation? Several high-tech methods member of the cytokine family, secreted by adipocytes,
have been devised, but for practical purposes the following regulates both sides of the energy equation—intake of food
measures are commonly used: and expenditure of energy. As discussed later, the net effect
of leptin is to reduce food intake and enhance the expenditure of
• Some expression of weight in relation to height, such as energy.
the measurement referred to as the body mass index (BMI)
= (weight in kilograms)/(height in meters)2, or kg/m2 In a simplified way the neurohumoral mechanisms that
regulate energy balance and body weight may be divided
• Skinfold measurements into three components (Fig. 7–23):
• Various body circumferences, particularly the waist-to-
• The peripheral or afferent system generates signals from
hip circumference ratio various sites. Its main components are leptin and adipo-
nectin produced by fat cells, insulin from the pancreas,
The BMI is closely correlated with body fat. BMIs in the ghrelin from the stomach, and peptide YY from the
range 18.5 to 25 kg/m2 are considered normal, while BMIs ileum and colon. Leptin reduces food intake and is
between 25 and 30 kg/m2 identify the overweight, and discussed in detail further on. Ghrelin secretion
BMIs greater than 30 kg/m2, the obese. It is generally stimulates appetite, and it may function as a “meal-
agreed that a BMI higher than 30 kg/m2 imparts a health initiating” signal. Peptide YY, which is released post-
risk. In the following discussion, for the sake of simplicity, prandially by endocrine cells in the ileum and colon, is
the term obesity is applied to both the overweight and the a satiety signal.
truly obese.
• The arcuate nucleus in the hypothalamus, which processes
The untoward effects of obesity are related not only to and integrates the peripheral signals and generates
the total body weight but also to the distribution of the new signals that are transmitted by (1) POMC
stored fat. Central, or visceral, obesity, in which fat accumu- (pro-opiomelanocortin) and CART (cocaine- and
lates in the trunk and in the abdominal cavity (in the mes- amphetamine-regulated transcript) neurons; and (2)
entery and around viscera), is associated with a much
higher risk for several diseases than is excess accumulation
of fat in a diffuse distribution in subcutaneous tissue.