Ebook Harrison''s endocrinology (3rd edition): Part 2
➤ Gửi thông báo lỗi ⚠️ Báo cáo tài liệu vi phạmNội dung chi tiết: Ebook Harrison''s endocrinology (3rd edition): Part 2
Ebook Harrison''s endocrinology (3rd edition): Part 2
SECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2food supplies are intermittent, the ability to store energy in excess of what is required for immediate use is essential lor survival. Fat cells, residing within widely distributed adipose tissue depots, are adapted to store excess energy efficiently as triglyceride and, when needed, to release stor Ebook Harrison''s endocrinology (3rd edition): Part 2ed energy as free fatty acids for use at other sites. This physiologic sys tern, orchestrated through endocrine and neural pathways. permits humans toEbook Harrison''s endocrinology (3rd edition): Part 2
survive starvation for as long as several monllis. i lowever, in the presence ol nutritional abundance and a sedentary' lifestyle, and influ cnced imSECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2 is a slate ol excess adipose tissue mass. Although often viewed as equivalent to increased body weight, this need nor be the case lean but very muscular individuals may be overweight by numerical standards without having increased adiposity. Body weights are distributed continuously in populations, Ebook Harrison''s endocrinology (3rd edition): Part 2 so that choice of a medically meaningful distinction between lean and obese is somewhat arbitrary. Obesity is therefore more effectively defined by aEbook Harrison''s endocrinology (3rd edition): Part 2
ssessing its linkage to morbidity or mortality.Although not a direct measure of adiposity, the most widely used methosl to gauge obesity is the bl'dy SECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2ckness), densitometry (underwater weighing). CT or MR1, and electrical impedance. Using data from the Metropolitan Life Tables, BMIs for ths' midpoint of all heights ansi frames among hath men and women range from 19 to 26 kg/nr; at a similar BMI, women have more body fat than men. Bases! on data of Ebook Harrison''s endocrinology (3rd edition): Part 2 substantial morbidity, a BMI of 30 is most commonly uses! as a threshold for obesity in bothmen and women, l^rgc scale epidemiologic studies suggestEbook Harrison''s endocrinology (3rd edition): Part 2
that all cause, metabolic, cancer, and cardiovas cular morbidity begin to rise (albeit al a slow rale) when BMls are >25. suggesting dial the culolf fSECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2MI between 25 and 30 should be viewed as medically significant and worthy of therapeutic intervention, especially in die presence of risk factors dial are inlluenced by adiposity such as hypertension and glucose intolerance.The distribution of adipose tissue in differcitt anatomic depots also has su Ebook Harrison''s endocrinology (3rd edition): Part 2bstantial implications for morbidity. Specifically, inlraabdominal and abdominal subcutaneous fat have more significance than subcutaneous fal presentEbook Harrison''s endocrinology (3rd edition): Part 2
in the buttocks and lower extremities. This distinction is most easily made clinically by determining the waist to hip ratio, with a ratio >0.9 in woSECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2emia, and hyperandrogenism in women, arc linked more strongly to intraabdominal and/or upper body fat than to overall adiposity (Chap. 18). The mechanism underlying this association is unknown but may relate to the fact that inlraabdonnn.il adipocytes are more lipolytically active than those from ot Ebook Harrison''s endocrinology (3rd edition): Part 2her depots. Release of free fatty acids into die portal circuit rion has adverse metabolic actions, especially on the liver. Whether adipokines and cyEbook Harrison''s endocrinology (3rd edition): Part 2
tokines secreted by visceral adipocytes play an additional role in systemic complications of obesity is an area of active investigation.PREVALENCEDataSECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2) has increases! from 14.5% (between 1976 and 1980) to 33.9% (between 2007 and 2008). As many234WeightHeight cm in.235Biology of obesityFIGURE 16-1Nomogram for determining body mass index. To use this nomogram, place a ruler or other straight edge between the body weight (without clothes) in kilogra Ebook Harrison''s endocrinology (3rd edition): Part 2ms or pounds located on the left-hand lino and the height (without shoes) incentimeters or inches located on the right-hand lino. The body mass indexEbook Harrison''s endocrinology (3rd edition): Part 2
is read from the middle of the scale and is in metric units. {Copyright 1979, George A. Bray, MD; used with permission.}as 68% OÍ U.S. adults aged >20SECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2opulation. I he increasing prevalence of medically significant obesity raises great concern. Obesity is more common among women ami III the poor, and among blacks and Hispanics; the prevalence in children is also rising at a worrisome rate.PHYSIOLOGIC REGULATION OF ENERGY BALANCESubstantial evidence Ebook Harrison''s endocrinology (3rd edition): Part 2 suggests that body weight is regulated by both endocrine and neural components that ultimately influence the effector arms of energy intakeand expendEbook Harrison''s endocrinology (3rd edition): Part 2
iture. This complex regulatory system is nec cssary because even small imbalances between energy intake and expenditure will ultimately have large effSECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2rgy balance cannot be monitored easily by caloric-counting in relation to physical activity. Rather, body weight regulation or dysregulation depends on a complex interplay of hormonal ami neural signals. Alterations in stable weight by forced overfeeding or food deprivation induce physiologic change Ebook Harrison''s endocrinology (3rd edition): Part 2s that resist these perturbations: with weight loss, appetite increases and energy expenditure falls; with overfeeding, appetite falls and energy expeEbook Harrison''s endocrinology (3rd edition): Part 2
nditure increases. This latter compensatory mechanism236 frequently fails, however, permitting obesity to develop when food is abundant and physical aSECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2ntly in the hypothalamus) to influence appetite, energy expenditure, and neuroendocrine function (see below).Appetite is influenced by many factors that are integrated by the brain, most importantly within the hypothalamus (big. 16-2). Signals that impinge on the hypothalamic center include neural a Ebook Harrison''s endocrinology (3rd edition): Part 2fferent*. hormones, and metabolites. Vagal inputs arc particularly important, bringing information from viscera, such as gut distention. I lormonal siEbook Harrison''s endocrinology (3rd edition): Part 2
gnals include leptin, insulin, cortisol, and gut peptides. Among the latter IS ghrelin. winch IS made 111 the stomach and stimulates feeding, and peptSECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2nd/or via the vagus nerve. Metabolites, including glucose, can influence appetite, as seen by the effect ol hypoglycemia to induce hunger; however, glucose is not normally a major regulator of appetite. These diverse hormonal, metabolic, and neural signals act by influencing rhe expression and relea Ebook Harrison''s endocrinology (3rd edition): Part 2se of various hypothalamic peptides |e.g.. neuropeptide Y (NPY). Agouti-related peptide (AgRP), a melanocyte stimulating hormone (a MSH), and melaninEbook Harrison''s endocrinology (3rd edition): Part 2
concentrating hormone (MCH)] that arc integrated with serotonergic, catccholamincrgic, endocannabinoid, and opioid signaling pathways (see below). PsySECTION IIIDIABETES MELLITUS, OBESITY, LIPOPROTEIN METABOLISMCHAPTER 16BIOLOGY OF OBESITYJeffrey s. Flier ■ Eleftheria Maratos-FlierIn a world where f Ebook Harrison''s endocrinology (3rd edition): Part 2, and theDiabetes Mellitus, Obesity, Lipoprotein MetabolismPsjv.liGọi ngay
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