About 2–3 g of protein has to be broken down to synthesize 1 g of glucose; about 20–30 g of protein is broken down each day to make 10 g of glucose to keep the brain alive. However, this number may decrease the longer the fasting period is continued, in order to conserve protein. Starvation ensues when the fat reserves are completely exhausted and protein is the only fuel source available to the body. Thus, after periods of starvation, the loss of body protein affects the function of important organs, and death results, even if there are still fat reserves left. In a leaner person, the fat reserves are depleted faster, and the protein, sooner, therefore death occurs sooner.) Ultimately, the cause of death is in general cardiac arrhythmia or cardiac arrest, brought on by tissue degradation and electrolyte imbalances. Conditions like metabolic acidosis may also kill starving people. Prevention
Starvation can be caused by factors beyond the control of the individual. The Rome Declaration on World Food Security outlines several policies aimed at increasing food security and, consequently, preventing starvation. These include:

Poverty reduction
Prevention of wars and political instability
Food aid
Agricultural sustainability
Reduction of economic inequalitySupporting farmers in areas of food insecurity through such measures as free or subsidized fertilizers and seeds increases food harvest and reduces food prices. Treatment
Patients that suffer from starvation can be treated, but this must be done cautiously to avoid refeeding syndrome. Rest and warmth must be provided and maintained. Food can be given gradually in small quantities.
Mauriac syndrome is a rare complication of type 1 diabetes characterized by extreme liver enlargement due to glycogen deposition, along with growth failure and delayed puberty. It occurs in some children and adolescents with type 1 diabetes irrespective of their glycemic control. History
Mauriac syndrome was first described in 1930 by Pierre Mauriac. It was described as a syndrome of growth failure and delayed puberty in children with poorly-controlled type I diabetes. Signs and symptoms
Patients with Mauriac syndrome may present with obesity, hepatomegaly, cushingoid facies, and elevated liver enzymes. Patients usually have growth failure and delayed puberty, which should warn the physician about insufficient management of the patients diabetes. These symptoms can be reversed with good glycemic control. Genetics
Abnormally high blood sugar levels are relatively common among patients with type I diabetes, but Mauriac syndrome is rare. This suggests that high blood sugar is not the only factor necessary to cause the syndrome. A study of an adolescent boy with severe Mauriac syndrome found a mutation in PHKG2, which is the catalytic subunit of the enzyme glycogen phosphorylase kinase (PhK). PhK is a large enzyme complex responsible for the activation of glycogen phosphorylase, the first enzyme in the pathway of glycogen metabolism. This childs mutation inhibited glycogen metabolism and caused increased glycogen deposition in the liver. The childs mother had the mutant enzyme, but no liver enlargement. The childs father had type 1 diabetes. Neither parent had Mauriac syndrome.