Type 2 diabetes in children and adolescents

 

 

 

Prophet Mohammed  (PBUH) said "order your children to pray when  they are seven and beat them when  they are ten and let them not to sleep in the same place in one bed .

Mystery behind type 2 diabetes

WHAT DO healthy adolescents and people with type 2 diabetes have in common? Both grow resistant to insulin, according to a new study by researchers at the Keck School of Medicine of USC and the University of Alabama at Birmingham (UAB).

Over the first few stages of puberty, cells in children's bodies respond less and less to insulin, a natural hormone that-among other things-helps cells convert sugar from food into energy, the authors write in the journal Diabetes. ``Puberty is a metabolically critical time,'' says Michael I. Goran, associate director of the USC Institute for Health Promotion and Disease Prevention Research and study co-author. Results of the study, the first to track sensitivity and response to insulin from childhood through young adulthood, carry implications for preventing type 2 diabetes during adolescence through steps such as diet and exercise.

Doctors are diagnosing increasing numbers of young adults with type 2 diabetes, a significant health problem nationwide. Insulin works in this way: Normally, after a meal, the body breaks down carbohydrates into glucose, or sugar, in the blood. That signals the pancreas to secrete insulin, because insulin helps the body's cells pick up the glucose and convert it to energy. But when cells become resistant or less sensitive to insulin, as they do in type 2 diabetes, they cannot absorb glucose as well as they should and the sugar remains in the blood. In healthy teens, insulin resistance disappears after puberty ends. Among people with type 2 diabetes, though, cells can ignore insulin more and more until they stop responding to insulin altogether.

The Diabetes study followed the development of 60 ethnically diverse children, beginning at about age nine. After two years, the children had progressed to various stages of puberty (measured by the appearance of sexual features). Among those who reached the middle stage puberty, sensitivity to insulin dropped by 32 per cent, report Goran, professor of preventive medicine at the Keck School, and Barbara Gower, assistant professor of nutrition sciences at UAB. Among those who did not yet show the signs of puberty, insulin sensitivity actually increased slightly. Researchers found no link between insulin resistance and the release of sex hormones such as testosterone during puberty. Nor were gender, ethnicity or body fat implicated as causes for that insulin resistance. Goran and Gower conclude that something about the changes of puberty-not simply aging-contributes to lowered sensitivity to insulin.

``The theory is that lowered sensitivity is a beneficial thing that switches on growth during puberty,'' Goran says. The tumultuous transformations and growth spurts of the teen years might naturally require the body to produce additional insulin to drive growth and tissue deposition. When muscle and other cells become less sensitive to insulin, the pancreas's beta cells (tiny insulin factories) usually respond by working harder to pump more insulin into the system, Goran explains. The sheer volume of insulin helps compensate for the body's inefficient use of it. Interestingly, though, the researchers found that in adolescents, beta cells do not produce as much insulin as expected to make up for insulin resistance.

That might be a protective function, Goran says. Here is why: In people with type 2 diabetes, beta cells appear to work harder and harder until they finally ``wear out.'' In contrast, in healthy teens, beta cells might relax somewhat during adolescence so that when insulin sensitivity returns to normal at the end of puberty, the beta cells are vital and can keep working throughout adulthood. Teen-agers who do not recover their insulin sensitivity by adulthood, though, may end up with type 2 diabetes.``In these teens, something makes them unable to recover,''Goran says. ``Something causes them to go beyond the threshold of insulin resistance that can be sustained and we need to continue tracking these children.'' Scientists have noted that children today tend to start puberty at younger ages-likely linked to high body fat during childhood-and that might play a role in not recovering from teen-age insulin resistance at the end of puberty.

At younger ages, children's bodies might not be ready to start a period of insulin resistance. When researchers determine the mechanisms for changes in insulin sensitivity during puberty, it may be important to find ways to ensure that insulin sensitivity recovers by the end of puberty and to protect beta cells

Comment :

1-     Growth Hormone

Gh low in infancy slightly higher in during childhood and dramatically increased during puberty Gh depend on insulin like growth factor because half life of Gh 20-30 minutes .But when it bound toIGF it increases to3-18Hthe IGF level at birth lower  than adult and rise gradually during childhood to reach the adulate rang by 8-10 years A number of hormones influence GH release most factors that stimulate GH release more potent in women than in men an effect mediated by estrogen Gh may act as an insulin antagonist inhibit glucose up take by tissues .Patients with GH deficiency are prone to insulin- induced hypoglycemia .Patients with GH excess develop insulin resistance .The factors which stimulate GH release stress .slow-wave sleep  and glucocorticoids

2- Testosterone

In the of one year testosterone remain low  in the onsets of puberty it begins to rise in boys and reach adult level in  age 17

3- ESTROGEN

With puberty the sensitivity of the hypothalamic-pituitary centers to circulating steroid hormones is decreasedLHRH release by the hypothalamus increases gnadadotropin secretion by the pituitary is enhanced ovarian estrogen secretion increases and the anatomic changes of puberty ensue At the age 10 –11 the first secondary sexual characteristic’s begin to appear in girls

I mention sex hormones and GH  may increase  insulin resistance and Puberty appears to play a major role in the development of type 2 diabetes in children. During puberty, there is increased resistance to the action of insulin, resulting in hyperinsulinemia (8). It has been known for many years that insulin responses during an OGTT increase significantly from the toddler ages to adolescence. After puberty, basal and stimulated insulin responses decline. Hyperinsulinemic-euglycemic clamp studies demonstrate that insulin-mediated glucose disposal is on average 30% lower in adolescents between Tanner stages II and IV compared with prepubertal children in Tanner stage I and compared with young adults. In the presence of normal pancreatic -cell function, puberty-related insulin resistance is compensated by increased insulin secretion.

Both growth hormone and sex steroids have been considered as candidates for causing insulin resistance during puberty. The fact that sex steroids remain elevated after puberty while insulin resistance decreases makes sex steroids an unlikely cause of insulin resistance. Conversely, mean growth hormone levels increase transiently during puberty coincidental with the decrease in insulin action. In addition, administering growth hormone to non–growth hormone–deficient adolescents is associated with deterioration in insulin action, while testosterone administration has no such effect. Thus, increased growth hormone secretion is most likely responsible for the insulin resistance during puberty, and both growth hormone secretion and insulin resistance decline with completion of puberty.

Given this information, it is not surprising that the peak age at presentation of type 2 diabetes in children coincides with the usual age of mid-puberty. In an individual who has a genetic predisposition for insulin resistance, compounded with environmental risk exposure, the additional burden of insulin resistance during puberty may tip the balance from a state of compensated hyperinsulinemia with normal glucose tolerance to inadequate insulin secretion and glucose intolerance that continues beyond puberty.

The adverse effect of obesity on glucose metabolism is evident early in childhood. In healthy white children, total adiposity accounts for ~55% of the variance in insulin sensitivity. Obese children are hyperinsulinemic and have ~40% lower insulin-stimulated glucose metabolism compared with non obese children. Moreover, the amount of visceral fat in obese adolescents is directly correlated with basal and glucose-stimulated hyperinsulinemia and inversely correlated with insulin sensitivity. In African-American children, as BMI increases, insulin-stimulated glucose metabolism decreases and fasting insulin levels increase. Furthermore, in these children, the inverse relationship between insulin sensitivity and abdominal fat is stronger for visceral than for subcutaneous fat. In a 7-year longitudinal study of African-American and white young adults 18 years and older, the strongest predictor for increases in both insulin and glucose concentrations was an increase in BMI.

I agree with the study that Type2 diabetes in adolescents has not any relation to gender or ethnicity because according to prophet [PBUH] order prayer for all Muslims without distinguish between races or sex

1- Five time daily prayer [controlling stress hormones ,exercise moderate  diet] this well  prevent insulin resistance and also will prevent hyperglycemia and  will be in normoglycemic state

2- When prophet  order us to not allow our children to sleep in the same bed .He is explaining and teaching parents and adolescents  how they should behave in the society about sex behavior In the same time he  protected them  by asking them who can marry should marry because it helps them in lower their  gaze and guard their modesty[;his privet parts from committing illegal sexual intercourse] And I compare  what is  written about adolescents sexual behavior  in USA to day Adolescents in the United States have a higher proportion of pregnancies that are unintended and that end in abortion than do adults.¹ Moreover, adolescents who have initiated sexual intercourse have some of the highest age-specific rates of sexually transmitted diseases (STDs),² which along with unintended pregnancy impose enormous costs in human pain and suffering, in social and economic opportunity, and in social welfare and health care.³ Early initiation of sexual intercourse, frequency of intercourse, number of sexual partners and use of condoms and other forms of contraception are key behavioral determinants of unintended pregnancy and STDs, including HIV.⁴ Recognizing the impact of these behaviors, the public health community has set national goals for delaying the initiation of intercourse, increasing abstinence among sexually experienced adolescents and increasing the use of condoms and other contraceptives.⁵