Hyperphagia can lead to significant morbidities (e.g., stomach rupture, obesity, diabetes, cardiovascular disease) and mortality (e.g., choking, accidental death due to food seeking behavior).
The most common and treatable form of monogenic obesity is due to mutations in the LEP gene manifesting as
hyperphagia and rapid weight gain starting from early infancy (4).
Van Assche et al., "Established diet-induced obesity in female rats leads to offspring
hyperphagia, adiposity and insulin resistance," Diabetologia, vol.
The WBKDF rat carries the fatty mutation (fa) in the leptin receptor gene, and homozygous animals (fa/fa) exhibit
hyperphagia and obesity, in addition to insulin resistance and glucose intolerance [5-8].
Gao et al., "The act of voluntary wheel running reverses dietary
hyperphagia and increases leptin signaling in ventral tegmental area of aged obese rats," Gerontology, vol.
Those include
hyperphagia [16], temper tantrums [17], obsessive-compulsive behaviors [18, 19], repetitive and ritualistic behaviors [20], self-injurious behaviors [21, 22], and hyperactive/impulsive behaviors [23].
hermaphoditum, are the most important food items during
hyperphagia, with lingonberry V.
It was shown that oestrogen decreases
hyperphagia via hypothalamic stimuli and furthermore leads to enhanced glucose tolerance, higher insulin sensitivity, and an improved [beta]-cell integrity [8].
However, the opposite was observed regarding the individual feed consumption per meal parameter (Figure 1B), indicating
hyperphagia in treatments where food frequency was lowest.
Leptin inhibits arcuate NPY production, and genetic knockout of NPY reduces
hyperphagia and obesity in ob/ob mice (38).
[14] Empirical evidence suggested that leptin hormone deficiency or leptin receptor resistance manifest with
hyperphagia, obesity, type 2 diabetes, and neuroendocrine disorders.
It should also be noted that the
hyperphagia and obesity associated with PWS do not present until late childhood.