Adipose tissue is commonly known as ‘body fat’ and is found over various body locations, like under the skin, around the organs, within the bone marrow, and breast tissues. The adipose tissue becomes active as an endocrine organ during puberty. Due to metabolic changes during puberty, the adipose tissue produces specific adipose-derived proteins called adipocytokines. Leptin, adiponectin, and resistin are the types of adipocytokines whose functions involve the metabolism of lipids and lipoproteins and vascular homeostasis. The essential adipocytokine is leptin, a satiety hormone. It balances the body energy by inhibiting food intake, induces puberty, and is directly linked to an increase in total body fat (TBF). Leptin is synthesized in the stomach, placenta, mammary glands, and ovaries. The leptin production shows sexual dimorphism, which is the variability in effects in males and females after the onset of puberty.
There is a three times higher production of leptin in females in comparison to males after the onset of puberty. The hips enlarge, and the waist to hip ratio decreases. More fat is deposited in the hip, thigh, and breast areas. Females develop a gynoid body, and there is increased deposition of subcutaneous fat tissue under the skin layer. Hence, girls who predominantly have fat become obese and overweight after puberty. There is more deposition of visceral fat around organs which increases insulin resistance and can cause ailments like type 2 diabetes in the future.
In males, there is lesser production of leptin in comparison to females. Males have an android body development, and unlike in females, the body fat is accumulated in the abdominal region and the fat-free mass (FFM) regions like skeletal muscles. The decreased leptin production in males is attributed to testosterone production, which inhibits leptin production up to some extent.
Changes in Lean Body Mass
Lean body mass (LBM) is the difference between the total body weight and the weight of body fat. More simply, lean body mass is the weight of everything, excluding fat weight. An adequate lean body mass is essential for good health. LBM at an older age is determined by LBM during puberty. LBM is at its peak during puberty and relies on genetic factors, hormonal changes, sexual maturation, and the nutritional status of the individual. The variations in LBM result from variations in adiposity, free fat mass, total body fat, and environmental factors. LBM also shows sexual dimorphism because males and females show various development of lean body mass. During puberty, males develop more significant amounts of lean body mass, whereas females gain more fat mass. The relative measurement of values like LBM, FFM, and TBF is essential to check the advancement of chronic disorders such as obesity, cardiovascular diseases, hypertension, and diabetes.
Changes in Bone Mineral Density
Bone is made up of collagen and calcium compounds like calcium carbonate and calcium phosphate. Both collagen and calcium are responsible for making the bones strong. The bone development is enhanced during infancy and puberty due to drastic bodily changes during this time.
Girls reach the peak of bone calcium deposition by the age of 12-13, whereas boys reach the same by age 14. There is a drastic reduction of bone mass in girls when they attain the age of 15.
In comparison, the bone mass in males continues to increase till age 18 and only decreases after they achieve their peak height. However, the peak bone density in both sexes is only achieved after the end of puberty.
Late menarche (onset of menstruation) in girls often leads to osteoporosis and high fracture risk in the future. Hence, calcium supplements during pre-puberty may shift the menarche.
Sex steroids are essential for bone maturation and maintenance of bone mineral density (BMD). The male and female bodies produce both hormones: estrogen and androgens, but in varying amounts. Hypogonadism, a condition in which the production of sex hormones is not adequate, can lead to osteoporosis. Estrogen hormone is responsible for new bone formation, bone mineralization, and long bone maturation.
Estrogen deficiency in males during puberty can cause an abnormally tall stature and a reduction in BMD.
Androgen deficiency in women during puberty can lead to decreased BMD in the hip and spinal area, which can be problematic in the future during pregnancy and labor.
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