Features of DM type 1 vs 2

Symptoms of hyperglycemia

Lipodystrophy at Insulin injection-site

It's a complication of insulin therapy. As insulin is injected subcutaneously, it causes either one of two reactions:

• It promotes lipid formation & adipose tissue hypertrophy at the site of injection. This will cause a "lump" of fat there which can resemble a benign tumor in appearance. This condition is called Lipohypertrophy (lipo-hyper-trophy).

• It causes an immune reaction which results in the production of insulin antibodies that will suppress insulin activity especially at the site of injection (where its concentration is high). This will cause down-regulation of fat production & atrophy of adipose tissue, therefore it's called Lipoatrophy. This condition was more common in the days of bovine & porcine insulin (insulin extracted from cows and pigs). Nowadays we use recombinant human insulin, which is much less likely to cause an immune reaction.

مثلما كلت، الـ lipohypertrophy حاليًا شائعة بين مرضى السكري نوع أول أكثر بهواي من الـ lipoatrophy لأن الأغلبية يستخدمون recombinant human insulin (HRI) وهالشي قلل إحتمالية حصول رد فعل مناعي قوي، مقارنةً بالـ bovine/porcine insulin اللي جنة نستخدمها بالثمانينات وقبلها.

الإستثناء الوحيد هو الـ Insulin lispro لأنه رغم كونه HRI بس مع هذا ممكن يسبب lipoatrophy أكثر من باقي الأنواع (اللي همين ممكن يسببون هالشي بس بنسبة أقل بهواي من Lispro وكلهم يسببوها بنسبة أقل بهواي من الـ Bovine/Porcine)

A case of lipoatrophy due to insulin lispro:
A 35-year-old woman transferred from regular insulin to insulin lispro, as she had developed unawareness of hypoglycemia. After 23 months she developed a circumscribed area of lipoatrophy about 3 cm in diameter at an injection site on the right thigh. Her anti-insulin antibodies were high (50%). Six months later incipient lipoatrophy was seen in the same area in the contralateral thigh and the first lesion remained unchanged, although no more insulin had been injected there. She was transferred to insulin aspart, which caused no changes over 6 months. The anti-insulin antibodies were then 31%.

It refers to periodic episodes of hyperglycemia occurring in the early morning hours in DM patients. The dawn phenomenon has been documented in both type 1 and type 2 DM and has been demonstrated in all age groups. For both type 1 and type 2 DM, its prevalence is estimated to exceed 50%.

Pathophysiology:
In the early morning there is a transient increase in both hepatic glycogenolysis and gluconeogenesis which could raise plasma glucose levels. In healthy individuals plasma insulin levels remain steady through the night, with only a small increase in insulin secretion before dawn. This increase serves to achieve supression of the hepatic glucose production, thereby hyperglycemia is prevented by this physiologic surge of insulin. Hence, the dawn phenomenon does not occur in patients without DM because they can secrete normal amounts of insulin to prevent it. 

There is a similar phenomenon that causes hyperglycemia in the early morning, it is called Somogyi Phenomenon

Somogyi phenomenon is similar to the dawn phenomenon in the sense that both of them cause hyperglycemia in early morning, but with one important difference: Somogyi is preceded by hypoglycemia during the late evening (induced by insulin) which then causes a counterregulatory hormone response that produces hyperglycemia in the early morning. 
The hormones implicated in this phenomenon are glucagon, epinephrine, growth hormone, and cortisol.

This phenomenon is actually less common than the dawn phenomenon. Some researchers even consider it rare.

باختصار:

The dawn phenomenon IS NOT PRECEDED by evening hypoglycemia.
The Somogyi phenomenon IS PRECEDED by evening hypoglycemia.

As for their similarity: they are both "early-morning hyperglycemia."

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