Adiposity, excess, effect

The answer is A. Recent research has revealed that excess visceral fat deposits secrete several factors that have direct effects on the brain as well as directly on muscle to produce peripheral insulin resistance. Some of these newly identified factors are leptin, re-sistin, and adiponectin, whose mechanisms of action are still under active investigation. Death of pancreatic beta cells is a hallmark feature of type 1 diabetes and may occur only in very advanced stages of type 2 diabetes. Excess adipose in the thighs and buttocks does not contribute as strongly to insulin resistance as does visceral fat, presumably due to a lower level of endocrine activity of such fat depots. Dysfunction of liver lipid metabolism is more a consequence of excess activity of adipose than a cause of insulin resistance. A sedentary lifestyle contributes to build-up of excess fat stores but does not act directly to induce insulin resistance. 

Somogyi effect, including rebound hyperglycemia with chronically excessive insulin dosages systemicallergic reaction, marked by rash, angioedema, and anaphylaxis lipodystrophy or depression at injection site due to breakdown of adipose tissue lipo-hypertrophy or accumulation of subcutaneous tissue at injection site due to inadequate site rotation Rare... 

Consequently, the most of the excess G6P appears to be converted to fatty acids in the muscle, so in this case a substantial DNL is taking place in the muscle cells [96, 107]. The fate of the fatty acids is unknown. They may be oxidized or, at least partly, stored in the muscle cells, or transported to the adipose tissues and stored there. An interesting effect of fatty acid production is that they may inhibit GLUT4 [108, 109], leading to a kind of insulin resistance. 

Infrequent Somogyi effect (rebound hyperglycemia) with chronically excessive insulin doses. Systemic allergic reaction (rash, angioedema, anaphylaxis), lipodystrophy (depression at injection site due to breakdown of adipose tissue), lipohypertrophy (accumulation of SC tissue at injection... 

The "central" deposition of fat in patients, such as Corti Solemia, with Cushing s "disease" or syndrome is not readily explained because GCs actually cause lipolysis in adipose tissue. The increased appetite caused by an excess of GC and the lipogenic effects of the hyperinsulinemia that accompanies the GC-induced chronic increase in blood glucose levels have been suggested as possible causes. Why the fat is deposited centrally under these circumstances, however, is not understood. This central deposition leads to the development of a large fat pad at the center of the upper back ("buffalo hump"), to accumulation of fat in the cheeks and jowls ("moon facies") and neck area, as well as a marked increase in abdominal fat. Simultaneously, there is a loss of adipose and muscle tissue below the elbows and knees, exaggerating the appearance of "central obesity" in Cushing s "disease" or syndrome. 

Vitamin A deficiency can have drastic consequences, as would be predicted from its importance in vision. Night blindness—and even total blindness—can result, especially in children. On the other hand, an excess of vitamin A can have harmful effects, such as bone fragility. Lipid-soluble compounds are not excreted as readily as water-soluble substances, and excessive amounts of hpid-soluble vitamins can accumulate in adipose tissue. 

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