Hypothalamic expression of the GCK gene plays an important role in the regulation of dietary glucose intake in particular, and overall feeding behavior in general. The primary hypothalamic cells expressing glucokinase are within the arcuate nucleus, ARC. Expression of the hypothalamic GCK gene increases specifically within the ARC in response to fasting. Manipulation of GCK expression within the ARC of experimental animals alters glucose intake. Increased GCK expression in the ARC results in increased glucose ingestion, whereas, decreased GCK expression results in reduced glucose ingestion. These observations indicate that ARC expression of GCK underlies the phenomenon of carbohydrate craving.
A vitamin is an organic compound needed in small quantities that cannot be made in cells. In human nutrition , most vitamins function as coenzymes after modification; for example, all water-soluble vitamins are phosphorylated or are coupled to nucleotides when they are used in cells.  Nicotinamide adenine dinucleotide (NAD + ), a derivative of vitamin B 3 ( niacin ), is an important coenzyme that acts as a hydrogen acceptor. Hundreds of separate types of dehydrogenases remove electrons from their substrates and reduce NAD + into NADH. This reduced form of the coenzyme is then a substrate for any of the reductases in the cell that need to reduce their substrates.  Nicotinamide adenine dinucleotide exists in two related forms in the cell, NADH and NADPH. The NAD + /NADH form is more important in catabolic reactions, while NADP + /NADPH is used in anabolic reactions.
Hartnup disorder is an autosomal recessive impairment of neutral amino acid transport affecting the kidney tubules and small intestine. The disorder results from defects in the specific transport system responsible for neutral amino acid transport across the brush-border membrane of renal and intestinal epithelium. Deficiencies in the solute carrier family 6 (neurotransmitter transporter), member 19 gene (symbol SLC6A19) are associated with Hartnup disorder. The encoded protein is also referred to as the system B(0) neutral amino acid transporter 1 [B(0)AT1] protein. The characteristic diagnostic feature of Hartnup disorder is a dramatic neutral hyperaminoaciduria. Additionally, individuals excrete indolic compounds that originate from the bacterial degradation of unabsorbed tryptophan. The reduced intestinal absorption and increased renal loss of tryptophan lead to a reduced availability of tryptophan for nicotinamide adenine dinucleotide (NAD + and NADP + ) biosynthesis. As a consequence affected individuals frequently exhibit pellegra-like rashes