It is stored in different depots to gynoid fat.Android fat cells are mostly visceral - they are large, deposited deep under the skin and are highly metabolically active. The hormones they secrete have direct access to the liver. The presence of fat in the trunk and upper body in males is facilitated by testosterone. Testosterone circulation causes fat cells to deposit around the abdominal and gluteofemoral region, whereas in women oestrogen circulation leads to fat deposits around areas such as thighs, breasts and buttocks. Therefore, measuring a persons oestrogen to testosterone ratio can reveal their predicted gynoid to android fat distribution. Android fat develops as a back-up source of energy when the male body is experiencing an imbalance, whereas gynoid fat develops after puberty, in order to better prepare the body for supporting a potential infant. 50% of the variance in abdominal fat mass observed in humans is due to genetic factors The cellular characteristics of adipose tissue in android and [gynoid] obese women are different. Android type have larger fat (hypertrophy) cells whereas gynoid type have increased number of fat cells (hyperplasia). This allows for hypertrophic obesity and hyperplastic obesity. Two different receptors, alpha and beta fat cell receptors, vary in their ability to facilitate or inhibit fat mobilization. Alpha-receptors are predominately in the lower body thus more abundant in gynoid patterns and Beta-receptors are predominantly in the upper body and so more abundant in android patterns.
: 811 With the classical, or neonatal presentation of glycine encephalopathy, the infant is born after an unremarkable pregnancy, but presents with lethargy, hypotonia, apneic seizures and myoclonic jerks, which can progress to apnea requiring artificial ventilation, and often death. Apneic patients can regain spontaneous respiration in their second to third week of life. After recovery from the initial episode, patients have intractable seizures and profound intellectual disability, remaining developmentally delayed. Some mothers comment retrospectively that they noticed fetal rhythmic "hiccuping" episodes during pregnancy, most likely reflecting seizure episodes in utero. Patients with the infantile form of glycine encephalopathy do not show lethargy and coma in the neonatal period, but often have a history of hypotonia. They often have seizures, which can range in severity and responsiveness to treatment, and they are typically developmentally delayed. Glycine encephalopathy can also present as a milder form with episodic seizures, ataxia, movement disorders, and gaze palsy during febrile illness. These patients are also developmentally delayed, to varying degrees. In the later onset form, patients typically have normal intellectual function, but present with spastic diplegia and optic atrophy. The mild form of the disorder corresponds to greatly reduced but not fully absent GCS activity.Transient neonatal hyperglycinemia has been described in a very small number of cases. Initially, these patients present with the same symptoms and laboratory results that are seen in the classical presentation.