Icreased Body Weight "Obesity"

Insulin as a accomplishable regulator of ob agent expression has also investigated. extra factors including glucocorticoids and adipogenic factors other than insulin, need that exploration (6).

Obesity pathogenesis is unknown. Zhang et al. investigated components of the physiological system that control frame weight. Positional cloning technologies were apply to isolate mouse obesity genes; genetic and physical maps were obtained, the gene was then isolated and the mutation detected. In mice, five single-gene mutations resulting in an obese phenotype have been described. The obese mutation (ob) was the first of the recessionary obesity mutations. Previous experiments with mutant and wild-type mice have shown ob mice to be deficient regarding a blood-borne factor that regulates nutrient intake and metamorphosis (8).

The authors report cloning and sequencing of the mouse ob gene and its serviceman homologue. "ob encodes a 4.5-kilobase (kb) adipose tissue messenger ribonucleic acid with a highly conserved 167-animo-acid open reading frame." The amino-acid era predicted is 84 percent identical between human beinge and mouse, with features of a secreted protein (8:425). Molecular and classical genetic markers show the mouse ob and db genes mapped to proximal chromosome 6 and midchromosome 4, respectively. If there are human homologs of ob and db, they are suggested

Lee, Proenca, Montez, Carroll, Darvishzadeh, Lee, and Friedman analyse abnormal splicing of the leptin sense organ. Mouse diabetes (db) gene mutations result in obesity and diabetes which resembles human obesity. Research suggests that the db gene "encodes the sensory receptor for the obese (ob) gene product, leptin" (5:632). The mutant protein, missing the cytoplasmic region, is believably to be defective in signal transduction. This points to the likelihood that weight-reducing set up of leptin could be mediated with signal transduction by a leptin receptor in the hypothalamus (5).

7. Maffei, M.; Fei, H.; Lee, G. H.; Dani,C.; Leroy, P.; Zhang, Y.; Proenca, R.; Negrel, R.; Ailhaur, G.; Friedman, J. M.

Increased expression in adipocytes of ob ribonucleic acid in mice with lesions of the hypothalamus and with mutations at the db locus. Proc. Natl. Acad. Sci. USA 92:6957-60.

The OB protein action site is reported as unknown. This protein demonstrates weight expiry due to effects regarding food intake (reduced) and ability expenditure. parallel bioactivity in mice and human OB proteins leads to the possibility that administering OB protein to macrocosm would have similar effects. Since the action of the OB protein was to make animals thinner, the authors purpose that it be called leptin, from the Greek root leptos, which means thin (4).

The ob gene is a molecule that is found to regulate energy balance in the mouse. Defects in this gene lead to an subjoin in adipose tissue mass which resembles obesity in humans. The ob gene in mice is researched in an effort to further understand physiologic pathways that regulate adiposity and body weight. ob gene product (OB protein) is expressed by all adipocytes in all adipose tissue depots and is important in the edict of body weight. Daily injections of this protein have been found to reduce body weight and adipose stores in mice. Comparable bioactivity in mice and human OB proteins leads to the possibility that administering
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