Analysis of Obesity Symptoms and Endocrine and Metabolic Disorders

Because of the thickened subcutaneous fat layer, obese people have a relatively small body surface area compared to their body weight, making it difficult to effectively dissipate body heat. This means their body temperature is not easily lost through radiation and conduction, but instead decreases through sweating to maintain a constant body temperature. Therefore, they are more sensitive to heat and sweat more than thinner people. Difficulty breathing: When obese individuals have more fat in their chest and abdomen, the abdominal wall thickens, the diaphragm rises, and ventilation becomes difficult. Excessive fat tissue accumulated below the diaphragm and in the chest wall compresses the lungs, causing shortness of breath and difficulty breathing even with minimal activity.

Joint pain: Due to gravity, joints suffer mechanical damage from prolonged exposure to excessive body weight, often appearing in the lower limb joints, such as the hip, knee, and ankle. There is also joint pain in the limbs caused by metabolic factors, such as abnormal purine metabolism and gout caused by increased plasma uric acid. Endocrine and metabolic disorders: Fasting and postprandial hyperinsulinemia, with baseline values ​​reaching 30 microunits/mL and postprandial values ​​reaching 300 microunits/mL, approximately twice the normal level. Due to a decrease in the number of insulin receptors in fat, muscle, and liver cells, patients are insensitive to insulin, often resulting in impaired glucose tolerance.

Total lipids, cholesterol, triglycerides, and free fatty acids are often elevated, indicating hyperlipidemia and hyperlipoproteinemia, which are the basis for inducing diabetes, atherosclerosis, coronary heart disease, and gallstones. Plasma amino acids and glucose tend to be elevated, forming a vicious cycle that stimulates pancreatic β cells and exacerbates obesity. Thyroid function is generally normal, but T3 may be high and T2 may be low when food intake is excessive, resulting in a low basal metabolic rate. Serum cortisol and 24-hour urinary 17-hydroxycorticosteroids may be elevated, but circadian rhythms and dexamethasone suppression tests are normal.

Growth hormone secretion decreases during starvation or hypoglycemia, weakening its role in promoting lipolysis. Female patients may experience amenorrhea, infertility, and virilization. Men may experience impotence. Pickwick syndrome (cor pulmonale syndrome) is a clinical syndrome of severe obesity. Excessive abdominal and chest wall fat tissue impairs respiratory movement, leading to poor lung ventilation, restricted gas exchange, carbon dioxide retention, and a blood carbon dioxide combining power exceeding the normal range, resulting in respiratory acidosis; elevated blood carbon dioxide partial pressure, decreased arterial blood oxygen saturation, decreased oxygen partial pressure, cyanosis, and polycythemia.

Simultaneously, venous return is stagnant, venous pressure rises, jugular veins become distended, the liver enlarges, pulmonary hypertension develops, and the right ventricular load increases. Due to the significant increase in adipose tissue, total circulating blood volume increases, cardiac output and stroke volume increase, further burdening the left ventricular load, leading to high-stroke-output heart failure, constituting Pickwick syndrome. Obese individuals present with dyspnea, inability to lie flat, intermittent or Cheyne-Stokes respiration, rapid pulse, and may experience cyanosis, edema, altered mental status, drowsiness, or stupor. Digestive system manifestations include persistently strong appetite, excessive hunger and overeating, frequent constipation and abdominal distension, and a fondness for snacks, sweets, pastries, and desserts.

Some obese individuals may experience palpitations, sweating, and hand tremors if they do not eat in time; those with gallstones may experience chronic indigestion and biliary colic; and hepatomegaly may occur in cases of hepatic steatosis. Complications include increased mortality: The mortality rate of obese individuals is significantly higher than that of those of normal weight, and the mortality rate increases with increasing weight. Studies have shown that obese individuals have a significantly higher mortality rate from diabetes compared to those of normal weight, at 38.3% (men) and 37.2% (women); followed by cirrhosis, appendicitis, and gallstones, with mortality rates approximately doubled in obese individuals; cardiovascular disease, kidney disease, and accidental deaths are also more common.

Hypertension: Obese individuals are more likely to develop hypertension than non-obese individuals. Obese individuals often have increased cardiac output and blood volume, but in obese individuals with normal blood pressure, peripheral vascular resistance is decreased, while in obese individuals with hypertension, peripheral vascular resistance is normal or increased. Hypertension is a significant factor contributing to the high mortality rate among obese individuals. Coronary Heart Disease: The incidence of coronary heart disease is far higher in obese individuals than in non-obese individuals. The reasons include: ① Excessive weight increases the burden on the heart and leads to hypertension. ② Obese individuals often prefer fatty foods, consuming excessive amounts of saturated fatty acids, which promotes the formation of atherosclerosis.

③ Hypertriglyceridemia, hypercholesterolemia, and hyperlipoproteinemia increase blood viscosity and coagulability, making patients more susceptible to atherosclerosis, microcirculatory disturbances, and coronary artery embolism. ④ Reduced physical activity weakens or reduces coronary collateral circulation; obesity increases the body weight burden, which is also one of the causes of heart failure in coronary heart disease. Diabetes: The incidence of type 2 diabetes is four times higher in obese adults than in non-obese adults. Obesity is often an early manifestation of diabetes; 40%–60% of type 2 diabetes patients who develop the disease in middle age or later have polyphagia and obesity at onset and in the early stages.

The incidence of diabetes is directly proportional to obesity. Obese patients often develop diabetes before the onset of the disease due to excessive food intake, which overstimulates beta cells and leads to decompensation. In obese individuals, adipose tissue is less sensitive to insulin; more insulin is required for glucose to enter the enlarged adipocyte membranes. Therefore, the more fat an individual has, the greater the insulin demand, overburdening beta cells and eventually causing their exhaustion, resulting in diabetes. Generally, in the early stages of obesity, fasting blood glucose is normal, but a glucose tolerance test may sometimes show a hypoglycemic reaction 3-4 hours after glucose intake, due to delayed hyperinsulinemia.

As the disease progresses, glucose tolerance gradually declines, with postprandial 2-hour blood glucose levels rising above normal, followed by fasting blood glucose, eventually leading to diabetes. Glucose tolerance may return to normal when weight is restored.