The role of ghrelin and leptin in pubertal obesity: a glucose tolerance test 

Ghrelin and leptin are two hormones that control human eating behavior. During the pubertal period, they are essential for metabolic indicators, one of which is the glucose tolerance test. Its importance is difficult to overestimate, as it is considered to be a kind of marker of the state of lipid metabolism in adolescents. Read about the study that assessed the lipid spectrum and the affiliation of ghrelin and leptin in this article.


  1. Purpose of experiment.
  2. The course of the experiment.
  3. BMI and lipid spectrum hormones.
  4. Ghrelin and leptin.
  5. Conclusions.

Purpose of experiment

Clinical tests proving the association of fat and metabolic hormones in adolescent obesity before and after the classical glucose tolerance test was the aim of the experiment. The main group consisted of 76 adolescents with different degrees of obesity and the control group consisted of 15 healthy young men.

Ghrelin and leptin levels were studied by enzyme immunoassay, lipids by spectrophotometry. Fasting blood serum concentration of adipose tissue hormones, pancreatic hormone, growth hormone, triglycerides, cholesterol, glucose were studied. The study made it possible to reliably see a decrease in ghrelin level and a tendency to an increase in growth hormone in the examined patients.

It is well known that overweight gain has recently reached almost epidemic proportions. The WHO speaks of nearly 2 billion overweight adults. The number of overweight adolescents is increasing: the incidence has increased tenfold in 50 years. This is the most urgent problem today, because it is at this age that a steady increase in obesity and associated endocrine and metabolic pathologies is recorded. Lipid layers are endocrine active and synthesize a number of peptide biosubstances. One of the most influential is leptin.

This hormone blocks hunger and insulin synthesis. Its antagonist is ghrelin, which is produced by the gastric mucosa and stimulates appetite in contrast to leptin. The aim of the study was to evaluate the mutual influence of ghrelin, leptin and metabolic changes in young obese people before and after the classical glucose tolerance test.

The course of the experiment

A total of 91 patients were examined, many of whom did not consider themselves obese and had no complaints.

The complaints were identified by actively questioning the patients:

  • nearly 60% had headaches;
  • more than 50% had shortness of breath and chest pain;
  • 30% had hyperhidrosis;
  • 4% had increased appetite;
  • 16% had persistent thirst;
  • 3% had vergtigo.

From a thorough survey, we know that more than 70% of patients noted disordered eating with eating before bedtime and overeating carbohydrates and fats, more than 80% recalled close relatives with obesity, 30% had a history of chronic tonsillitis, 9% emphasized the association of excess weight gain with a tonsillectomy, and 5% had experienced a concussion. Only 14% had no association of excessive weight gain with genetic predisposition or previous illness.

In the study group, all patients were diagnosed with progressive obesity, with a quarter of the patients having been overweight since childhood and developing gradually, and 60% having developed it during puberty. A quarter of the patients noted weight gain with decreased motor activity or with a high-calorie diet. Almost all of the young men suffered from gynecomastia.

BMI and lipid spectrum hormones

Body mass index (BMI) was calculated using the formula: BMI=body weight in kg/height in m2.

When determining the degree of obesity, the WHO recommendations were used:

  • at BMI from 25.0 to 30.0 kg/m2, overweight was diagnosed;
  • BMI 30.0 to 35.0 kg/m2 was diagnosed as grade I obesity;
  • at BMI of 35.0 to 40.0 kg/m2 – degree II;
  • at BMI ≥40 kg/m2 – grade III.

In the study group, degree I obesity was detected in 31 patients, degree II in 30 patients, and degree III in 10 patients. Excessive body weight was found in 5 patients. The waist circumference (WC) to hip circumference (WC) ratio was used to assess the character of fat distribution. If it was more than 1, the young men were considered to be of abdominal obesity type. Obesity was gluteofemoral in 83% and abdominal in only 17%. The duration of the pathology ranged from 5 to 14 years.

Ten patients underwent a standard oral glucose tolerance test in the morning on a three-day diet with less restriction and normal physical effort, preceded by an overnight 10-12-hour fast. After blood sampling on an empty stomach to determine levels of hormones such as insulin, cholesterol, and adipose tissue hormones of interest, the patient drank 75 g of anhydrous glucose dissolved in a glass of water for no more than 5 minutes. Repeated blood sampling was performed one hour and two hours later, respectively. Diagnosis of carbohydrate metabolism disorders was performed according to WHO criteria.

Ghrelin and leptin

Levels of ghrelin and leptin, insulin, and growth hormone were assessed by ELISA; lipid levels were assessed spectrophotometrically. Glucose was monitored by glucose oxidase method. Insulin resistance index was calculated by the method of the ratio of glucose to insulin levels taken on an empty stomach. Statistics were performed using variation and correlation methods. Total cholesterol content in obese patients did not differ from that in the control group.

Triglyceride and low-density cholesterol levels tended to increase. At the same time, high-density cholesterol significantly decreased. This also explains the increase of atherogenicity coefficient. An increase in glycemia within the normal range was ascertained. A drop in Caro index indicates insulin resistance. Adolescents with extra pounds have lower ghrelin levels compared with the control group.

A drop in ghrelin is accompanied by an increase in growth hormone concentration. In obese adolescents, a minimal correlation of leptin with insulin and an inverse relationship with the Caro index were found. This means that leptin is involved in the mechanisms of insulin resistance development, but is not the main trigger of the process. The glucose tolerance test conducted tells us that ingestion of glucose, which is similar to eating, does not block ghrelin synthesis and transport into the bloodstream, but increases growth hormone, which is presumably a variant of the development of obesity in puberty.


The study made it possible to come to the following conclusions:

  1. Young men with obesity and excess body weight are diagnosed with increased insulin synthesis and a fall in the Caro index, indicating the development of insulin resistance.
  2. Patients with excess body weight give a drop in ghrelin levels and an increase in growth hormone. At the same time, neither ghrelin nor growth hormone levels change, suggesting that these biologically active substances are involved in the development of adolescent obesity.
  3. The normal response of leptin to contact with glucose is impaired in obese and overweight adolescents.

Thus, the clinical study answered a number of questions that relate to the involvement of ghrelin and leptin in adolescent obesity.

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