As pointed out by you, carbohydrates are chiral molecules since they have carbon atoms carrying four different groups and the molecule cannot be superimposed upon its mirror image. The chiral molecule and its mirror image (enantiomers) may exist as a pair – a right handed D form or a left handed L form. The monosaccharides that are utilized by nature are of the D- absolute configuration and D-Glucose (dextrose or blood sugar) is the most widely occurring of all monosaccharides. Nearly all living organisms utilise only D-glucose as a source of energy for all biochemical reactions.
Practically all carbohydrates ingested in the diet are converted to glucose following transport to the liver. Catabolism of dietary or cellular proteins generates carbon atoms that can be utilized for glucose synthesis via gluconeogenesis. Additionally, other tissues besides the liver that incompletely oxidize glucose (predominantly skeletal muscle and erythrocytes) provide lactate that can be converted to glucose via gluconeogenesis.
Somogyi effect is the marked increase in fasting plasma glucose with an increase in plasma ketones. The hypoglycemia induced by insulin causes a counter-regulatory hormone response that produces hyperglycaemia. Unappreciated nocturnal hypoglycemia can lead to morning hyperglycaemia, and the physician or patient may increase the evening insulin, exacerbating the problem. The ability to suppress insulin release is an important physiologic response that people with insulin-requiring diabetes cannot carry out. Defence against hypoglycemia involves counter-regulatory hormones (glucagon, epinephrine, cortisol & growth hormone) which stimulate gluconeogenesis and glycogenolysis and counteract the anabolic effects of insulin. Recent research has questioned the importance of counter-regulatory hormones in mediating glycemic rebound. Hypoinsulinemia (waning of the insulin dose), insulin resistance, and hypersensitivity to the effects of the counter-hormones also may play a role.
Dawn phenomenon is the normal tendency of the blood glucose to rise in the early morning before breakfast. This rise in glucose, which may be due to the nocturnal spikes in growth hormone causing insulin resistance, probably is enhanced by increased hepatic gluconeogenesis secondary to the diurnal rise in serum cortisol.
Thus, both the dawn and Somogyi phenomena are characterized by morning hyperglycaemia, but the latter is due to rebound (counter-regulation) hyperglycaemia. In cases of dawn phenomenon, the patient should check blood glucose levels at 2-4 A.M. Administering intermediate insulin at bedtime can ameliorate the dawn and Somogyi phenomena.