Mechanisms of obesity in relation to diabetes, hypertension, and hyperlipidemia

Diabetes is classified into two types: type 1 and type 2 diabetes.

Type 1 diabetes mostly occurs in adolescents under the age of 15. It is also known as juvenile diabetes or insulin-dependent diabetes. This type of diabetes is mainly caused by genetic factors. It is caused by an obstruction of insulin secretion, resulting in an absolute lack of insulin, and is not related to obesity.

Type 2 diabetes usually develops slowly after age 40 and is also known as adult-onset diabetes or non-insulin-dependent diabetes mellitus.

These types of diabetic patients often have a history of obesity before the onset of the disease, and their blood insulin concentration is often higher than that of normal people. The lack of insulin is relative.

Patients with type 2 diabetes show different clinical characteristics depending on their obesity status: obese diabetic patients have elevated fasting blood insulin levels, while non-obese diabetic patients do not have elevated fasting blood insulin levels.

Therefore, it is more accurate to say that elevated blood insulin levels are related to obesity than diabetes. Thus, we have reason to believe that obesity is an important contributing factor to adult-onset diabetes.

In the case of obesity and diabetes, insulin secretion is reduced compared to obesity without diabetes, but is normal or even increased compared to healthy individuals.

In obese diabetic patients, insulin deficiency is relative.

This is because the cells of obese people are not sensitive to insulin. In order to meet the needs of metabolism, the pancreas must secrete 5 to 10 times more insulin than normal. If the secretion level is not high enough, blood glucose cannot be quickly and timely transferred to tissue cells, and blood sugar remains at a high level for a long time, which manifests as diabetes.

In obese individuals, cells are less sensitive to insulin, resulting in the utilization of less glucose, which in turn causes (or exacerbates) hyperglycemia and leads to (or exacerbates) hyperinsulinemia.

After insulin is distributed to cells throughout the body via the bloodstream, it acts on specific insulin receptors on the cell membrane. Hyperinsulinemia reduces the number of insulin receptors or weakens their affinity in target cells (mainly muscle tissues, while adipose tissues still respond normally to insulin) through "downregulation" (the regulation of hormone receptors by increased hormone concentration).

In other words, although obese patients have high plasma insulin concentrations, their blood sugar-lowering effect is poor, a condition clinically known as insulin resistance.

When obesity is reduced through dietary control, the number and affinity of receptors can return to near normal, the binding affinity to insulin also returns to normal, and blood sugar decreases accordingly.

However, if food intake is increased after treatment, insulin will be secreted in large quantities again, and insulin resistance may recur.

Therefore, the treatment of obese diabetic patients should focus on controlling their diet and reducing obesity.

In conclusion, to prevent the occurrence and development of diabetes, actively and effectively controlling diabetes and eliminating obesity are the most effective measures.

(II) Hypertension

Most obese patients also have hypertension. The incidence of hypertension in obese people can reach 22.3% to 52.0%, which is significantly higher than that in people of normal weight.

Moreover, the incidence of hypertension increases exponentially with increasing obesity levels.

According to some statistics, when the body weight is less than 10% overweight, the incidence of hypertension is 10.3%; when the body weight is 10% to 20% overweight, the incidence of hypertension is 19.1%, almost doubling; and when the body weight is 30% to 50% overweight, the incidence of hypertension can be as high as 56%.

In other words, a moderately obese person (overweight by 30% to 50%) is more than 5 times more likely to develop hypertension than someone who is less than 10% overweight, and 2.2 times more likely than someone who is mildly obese.

The prevalence of the disease among normal adults in my country is only 3% to 10%, with an average of 7.8%.

It is obvious that the more obese a person is, the higher the incidence of high blood pressure.

In obese patients with hypertension, both diastolic and systolic blood pressure are elevated, and the degree of elevation is parallel to the degree of obesity.

A study observed 567 obese men, of whom 84 (15%) had diastolic blood pressure >13.3 kPa, while among 1225 men of normal weight, only 70 (6%) had diastolic blood pressure >13.3 kPa. (The World Health Organization defines hypertension as systolic blood pressure >21 kPa and diastolic blood pressure equal to or greater than 13 kPa, either of which, once verified, constitutes hypertension.)

Obesity and hypertension pose a significant threat to children and adolescents. Some studies have shown that obese children are 2 to 3 times more likely to develop hypertension than normal children.

A study of over 1,000 obese school-aged children aged 10 to 13 found that 19.7% of them had a diastolic blood pressure greater than or equal to 11.3 kPa, compared to only 9.2% of normal-weight children with a diastolic blood pressure greater than or equal to 11.3 kPa.

Obesity complicated by hypertension may have the following causes: ① Obese patients have a large increase in adipose tissue, which can lead to an enlarged vascular bed and a corresponding increase in blood circulation.

Therefore, under normal heart rate, the cardiac output per minute and stroke volume are significantly increased, and the heart is overburdened for a long time, leading to left ventricular hypertrophy and high blood pressure.

② Obese patients have hyperadrenocortical function and a certain degree of water retention, which further increases blood circulation and exacerbates hypertension.

Obese patients with concurrent hypertension often experience spontaneous remission of hypertension after weight loss through a low-calorie diet, demonstrating the close relationship between obesity and hypertension.

(III) Hyperlipidemia

In layman's terms, hyperlipidemia refers to an abnormal increase in cholesterol or triglycerides in the blood, exceeding the normal range.

Hyperlipidemia is closely related to obesity.

Increased fat synthesis is the material basis for obesity.

Therefore, obese patients generally have lipid metabolism disorders, which are manifested as increased triglycerides and cholesterol in the blood (labeled as TG and TC on the test report), increased very low-density lipoprotein (pre-β-lipoprotein) and free fatty acids, and decreased high-density lipoprotein.

Although not all patients with hyperlipidemia are obese, only patients with type IB and type V hyperlipidemia are more likely to be obese. However, these two types are the most common in the population, so there are more obese patients than non-obese patients with hyperlipidemia.

Triglycerides and cholesterol are both fat-soluble substances. In order to be transported in the blood (which is water-soluble), they bind to proteins.

Proteins that transport triglycerides and cholesterol are called apolipoproteins, and the products of their binding are called lipoproteins.

Therefore, elevated blood lipids refer to changes in lipoproteins rich in cholesterol and/or triglycerides. Type β-II is hyperβ-lipoproteinemia (elevated low-density lipoprotein in the blood), and type N is hyperpreβ-lipoproteinemia (elevated very low-density lipoprotein in the blood).

Obese individuals have increased body fat, especially abdominal fat accumulation, which leads to excessive production of free fatty acids. These fatty acids flow into the liver via the portal vein system, increasing the synthesis and decreasing the degradation of very low-density lipoprotein (VLDL), resulting in increased VLDL levels in the blood and causing hyperpre-β lipoproteinemia (IN type).

Hyperinsulinemia in obese individuals promotes fat synthesis, while hyperlipidemia, in turn, increases insulin resistance, creating a vicious cycle.

Increased fat synthesis not only leads to an expansion of the cholesterol pool, but also promotes increased cholesterol synthesis and excretion, resulting in elevated low-density lipoprotein concentration in the blood and causing hyperβ-lipoproteinemia (type B).

The binding of adipocytes to high-density lipoprotein (HDL) is related to adipocyte size.

Hypertrophic adipocytes enhance the interaction with HDL, leading to a decrease in HDL concentration.

HDL transports cholesterol from peripheral tissues to the liver, where it is processed and excreted as bile acids. A decrease in HDL exacerbates hyperbeta-lipoproteinemia.

Obese patients can lose weight through diet reduction and exercise, which can alleviate or even restore hyperlipidemia to normal levels, further illustrating the relationship between the two.