mRNA expression of LEPR, JAK2, STAT3, NPY, KISS1 and TRPC5 in hypothalamus tissue
It appears leptin activates KISS1, TRPC5 in the hypothalamus tissue via LEPR through JAK2/STAT3 signal pathways in the hypothalamus of sheep at the onset of puberty.
Specifically, LEPR gene experienced a dramatically overexpression level at the puberty onset stage.
Furthermore, in order to detect whether leptin from adipose tissue could transduce signals to the brain tissue, we detected LEPR, JAK2, STAT3, NYP, KISS1, and TRPC5 in the hypothalamic tissue of goat at the onset of puberty, and prepubertal stage.
It is observed that leptin, LEPR, and JAK2, STAT3 were up-regulated in the puberty onset stage.
It is, therefore, necessary to carry out furthermore studies to identify possible mechanisms of leptin or LEPR that may link the changes in adipose and hypothalamus with the timing of puberty.
The frequencies of the LEP and LEPR genotype in control and acromegalic patients were shown in table 2.
The frequency of the genotype LEPR gene in patients and control groups did not show a significant deviation from the Hardy-Weinberg equilibrium.
No statistically significant difference was found among LEPR gene genotype groups (GG, GA and AA), as concerning BMI, SBP, DBP, fasting plasma glucose, IGF-I, GH, IGFBP3, triglyceride, total cholesterol, HDL and LDL cholesterol, right cIMT and plasma leptin level in patients and control individuals (Table 4).
In this study it was revealed that there was no statistically significant difference between acromegaly and control group for LEP A2548G genotypes and alleles; however, a statistically significant difference was observed between these groups for LEPR 223 genotypes and alleles distribution in our population.
Also, there was no significant difference among leptin levels of LEPR gene 223 genotypes groups in acromegalic and healthy subjects.
However, when the characteristics of LEPR gene in patients and control group were compared, left cIMT significantly increased in GG genotype group vs.