The impact of obesity on fatty liver, brain function, and children's growth and development

49. What is the relationship between obesity and fatty liver disease?

Under normal circumstances, fat absorbed by the intestines is broken down and converted in the liver, and then transported to adipose tissue for storage.

When the body is hungry, stored fat is mobilized to the liver or other tissues for breakdown and utilization.

Liver cells have a certain compensatory capacity and can adapt to the changing needs of the human body. In order to maintain constant blood sugar levels, after meals, when blood sugar concentration rises, most of the glucose is synthesized into liver glycogen and muscle glycogen and stored in the liver.

When fasting, liver glycogen is immediately broken down into glucose and enters the bloodstream, raising blood sugar levels and achieving a balance between fat synthesis, conversion, and utilization.

In obese patients, long-term energy intake exceeds consumption, leading to fat synthesis exceeding consumption and exceeding the liver cell's capacity. In addition, reduced insulin efficacy and impaired fat breakdown and utilization in the liver, such as insufficient synthesis of phospholipids or proteins, result in fat accumulation in liver cells, forming fatty liver.

Obese people often have fatty liver, even children.

The only difference lies in the severity of the impact, which is influenced by the course of the disease, the degree of obesity, and the level of disorder in body fat and glucose metabolism.

In 1994, the First Affiliated Hospital of Zhejiang University School of Medicine reported that using B-mode ultrasound to detect fatty liver, among 3015 employees, 576 (19.1%) were overweight and 94 (16.3%) had fatty liver; among 2439 non-overweight individuals, 63 (2.58%) had fatty liver. The prevalence of fatty liver in overweight individuals was 6.32 times that in non-overweight individuals.

After developing fatty liver, symptoms may include general weakness, abdominal distension, loss of appetite, and discomfort in the liver area.

Examination may reveal varying degrees of liver enlargement, with a smooth surface, blunt edges, and tenderness upon touch.

Blood tests may show changes in liver function, some patients may have hepatitis B, or elevated blood lipids. In addition, B-mode ultrasound can also indicate specific waveform changes in the liver.

Early or mild to moderate fatty liver is mostly reversible. That is to say, by losing weight and adjusting dietary intake to maintain a balance, fatty liver can improve or even disappear.

In severe cases, fatty liver disease may occur, presenting with nonspecific abdominal pain and abnormal liver function.

In later stages, increased fibrosis can lead to liver cirrhosis.

Does obesity affect brain function?

Obese individuals have abnormal sugar and fat metabolism, which can increase the risk of cerebral arteriosclerosis and lipid deposition in blood vessel walls. In addition, hypertension affects hemodynamics, such as increasing the oxygen difference between arteries, which is more pronounced during activity or stress.

Cardiac output increases, and blood volume increases.

There are also endocrine changes, such as increased adrenaline levels in obese individuals, imbalance of the renin-angiotensin-aldosterone system, hyperinsulinemia, increased thyroid hormone levels, increased adrenaline concentration (more than 30% higher than in non-obese individuals of the same age), increased aldosterone, and increased norepinephrine secretion. All of these can lead to elevated blood pressure, resulting in a higher incidence of cerebral hemorrhage or cerebral vascular occlusion and obstruction compared to non-obese individuals.

Abnormal sugar and fat metabolism can increase blood viscosity, reduce the oxygen-carrying capacity of red blood cells, and cause varying degrees of hypoxia in brain cells.

Obese patients experience more pronounced symptoms of hypoxia, including drowsiness, memory loss, and sluggish responses to external stimuli.

If accompanied by pulmonary heart syndrome and hypoxemia, altered consciousness may also occur.

Reports indicate that obese patients have abnormal secretion of various neuropeptides, including some neurotransmitters such as serotonin, β-endorphin, and pancreatic polypeptide.

The effects of these abnormally secreted substances on brain function are unclear, but they usually return to normal after weight loss.

No evidence has been found that they cause obesity, so they are currently considered to be secondary changes to obesity.

What are the effects of obesity on the endocrine system?

Obese patients are often referred to endocrinologists for diagnosis and treatment.

In reality, symptomatic obesity caused by endocrine disorders is very rare, while endocrine disorders caused by obesity are common.

Obesity can cause excessive insulin secretion, leading to abnormal sex hormone secretion and resulting in corresponding functional and metabolic disorders.

In addition, obese patients show a reduced secretory response of pituitary growth hormone and prolactin to physiological stimuli (hypoglycemia); enhanced conversion of adrenocortical hormones; elevated parathyroid hormone levels; increased levels of some gastrointestinal hormones (endorphins, enteropressin, neurotensin, vasodilator intestinal peptide), while others (gastrin, motilin) ​​remain normal; a slower response of hypothalamic antidiuretic hormone to water load; and higher responses of aldosterone and renin to furosemide stimulation compared to normal individuals.

These changes can improve on their own after adjusting and improving dietary balance, increasing exercise, and losing weight.

What impact does obesity have on children's growth and development?

Growth mainly refers to the development of the body at various ages before adulthood.

A person's growth is influenced by many factors, such as genetics, health status, exercise, and nutrition, but the most important factor is growth hormone secreted by the pituitary gland.

Obese people are all overnourished. Before adulthood, simple obesity is unlikely to develop to the point of affecting growth.

In the absence of genetic defects and hypothalamic or pituitary dysfunction, the growth of obese children is generally not greatly affected. Although studies have reported that obese children have a low response to growth hormone-releasing hormone (GHRH) from the hypothalamus, hypoglycemia, and exercise stimulation, their basal secretion levels are not significantly different from those of children of normal weight.

In addition, the growth-promoting effect caused by increased insulin levels means that obese children are similar in height to their peers with normal weight, and some children may even be taller than average.

While obesity does not significantly affect children's growth and development, excessively obese children may experience increased estrogen synthesis due to enhanced lipid metabolism, which can cause pre-pubertal menarche in obese girls; and in boys, facial skin may become smoother, hair may be less, testicular development may be poor or secondary sexual characteristics may not develop, and female-like physical changes may occur, such as excessive fat in the chest and abdomen, and fat accumulation in the chest resembling female breast development (without breast tissue).

Due to the influence of fat on sex hormone metabolism, obese children may experience puberty earlier, their bones may close earlier, and their final height will be shorter than that of children of normal weight at the same age.

Studies on serum growth hormone concentrations in obese children have been reported in recent years.

In 1994, Jinan Central Hospital conducted a comparative study on serum growth hormone levels in 73 obese adolescents aged 7-15 years and 63 normal adolescents. The obese group had a growth hormone level of 6.94±3.63 ng/ml, while the normal group had a growth hormone level of 13.24±4.72 ng/ml, showing a highly significant difference.

Obese adolescents have significantly lower serum growth hormone levels than normal individuals. Therefore, in general, obesity does have a certain impact on a child's height.