Ob ob db db

In all cases the dbdb and obob mutant conditions resulted in a depressed cellular accumulation of radiolabeled estradiol in both CNS and peripheral tissues relative to normal mice. Magnetic resonance imaging 31P magnetic resonance spectroscopy MRS 1H MRS and 18F-fluorodeoxyglucose-positron emission tomography PET were applied to measure cardiac function energy status lipid content and glucose uptake.

Identification of the gene mutated in ob led to the discovery of the hormone leptin which is important in the control of appetite.

Ob ob db db. Pathology of the liver in obese and diabetic obob and dbdb mice fed a standard or high-calorie diet. Non-alcoholic fatty liver disease NAFLD is one of the commonest liver diseases in Western countries. Although leptin deficient obob and dbdb mice are frequently used as murine models of NAFLD an exhaustive characterization of their hepatic lesions has not been reported to date particularly und.

In all cases the dbdb and obob mutant conditions resulted in a depressed cellular accumulation of radiolabeled estradiol in both CNS and peripheral tissues relative to normal mice. The obob mutation resulted in a more severe depression of tissue estradiol uptake than did the dbdb mutation. These studies indicate that the abnormal metabolic and hormonal states induced by the.

Genetically obese C57B16J-m dbdb mice were parabiosed with either lean male db or obese female obob mice. Male dbdb mice had lower serum leptin than females and this was reflected in the amount of protein that crossed the parabiotic union into their partners. Eighteen days post operation obob partners of dbdb mice had increased body temperature lost 50 body weight and.

Both obob and dbdb mice model phase I and phase II diabetes but only on the C57BLKSJ background do they progress to phase III. KK-A y is another diabetes model whose obesity is driven by hyperphagia. The mice however do not become as morbidly obese as obob and dbdb mice.

In addition to the obob mutation there is the diabetic dbdb mouse that also displays deficits in leptin signaling as there is a mutation to the leptin receptor Bahary et al 1990. Hummel et al 1966. The dbdb mouse develops early onset obesity characterized by hyperphagia and lack of activity Hummel et al 1966.

Importantly these animal models were used to understand the immediate and downstream. Leptin signaling-deficient obob and dbdb mice are hypogonadal. These mouse models should thus display an increase in bone resorption.

Indeed osteoclast numbers and bone resorption parameters are elevated in obob and dbdb mice 8. Nevertheless histomorphometric analyses of leptin signaling-deficient mice at various ages demonstrated that they have a higher bone mass than their wild-type. The diabetic mouse dbdb develops severe and potentially fatal diabetes due to a mutational inactivation of the leptin receptor gene 101 102.

The mouse strain was initially developed by Hummel et al. In 1959 by discovering a Lepr db mutation in mice with a C57BLKS background. The phenotype of the homozygous mice includes obesity insulin resistance and diabetes with secondary derangement.

Często zastanawiam się czy wychodzić naprzeciw klientom z reklamą. Dziś naszłam mnie dość typowa analogia do tematu. Każdy z nas pewnie rzucił monetę dla ulicznego grajka z prozaicznego powodu grał a nam się to spodobało także go doceniliśmy.

The obob and dbdb mice are extensively used as models in studies on the pathogenesis of these diseases. The goal of this study is to characterize the composition and structure of gut microbiota in these model mice at different ages. High-throughput sequencing was used to obtain the sequences of the highly variable 16S rRNA V3-V4 region from fecal samples.

The influences of single-gene missense mutations expressing either diabetes dbdb or obese obob metabolic syndromes on vertebral maturation and development in C57BLKsJ mice were evaluated by radiological and macro-morphometric analysis of the resulting variances in osteodevelopment indices relative to control parameters between 8 and 16 weeks of age syndrome. In summary impaired muscle regeneration in obob and dbdb mice was associated with reduced macrophage accumulation angiogenesis and myoblast activity and could have implications for insulin sensitivity in the skeletal muscle of obese and type 2 diabetic patients. The obob or obese mouse is a mutant mouse that eats excessively due to mutations in the gene responsible for the production of leptin and becomes profoundly obese.

It is an animal model of type II diabetes. Identification of the gene mutated in ob led to the discovery of the hormone leptin which is important in the control of appetite. Both obob and dbdb mouse models have defective leptin signallingwithalackofleptinexpressioninobobmiceanda leptin-receptor deficiency in dbdb mice.

Most importantly owing to their different genetic backgrounds they possess different susceptibilities to develop diabetes. The obob mice on the C57BL6J background are able to compensate for IR. The dbdb mouse is a model of obesity diabetes and dyslipidemia wherein leptin receptor activity is deficient because the mice are homozygous for a point mutation in the gene for the leptin receptor.

In dbdb mice induced swimming helped to overcome obesity by upregulating uncoupling proteins. Leptin receptor and pregnancy. Two obese mouse models were studied.

One exclusively with obesity obob and another with type 2 diabetes dbdb. Both models have impaired leptin signalling as a cause for obesity but the different genetic backgrounds determine the susceptibility to diabetes. To the best of our knowledge here we reported for the first time the underlying mechanistic therapeutic efficacy of the novel osmotin a homolog of mammalian adiponectin against NAFLD in leptin-deficient obob and dbdb mice.

The obob and dbdb mice were treated with osmotin at a dose of 5 μgg three times a week for two weeks. To co-relate the in vivo results we used the human. The db and ob mutations produced different effects on the content and fragmentation of the IR proteins and on insulin signalling.

The db and ob mutation-induced downregulation of α- and β subunits decreased IR in the interstitium. Conversely in tubules and the anterior pituitary the α subunit was not affected but the reduced β subunits to be activated by insulin would not suffice to stimulate. Transverse aortic constriction TAC was performed in non-diabetic db and diabetic dbdb mice to induce pressure overload.

Magnetic resonance imaging 31P magnetic resonance spectroscopy MRS 1H MRS and 18F-fluorodeoxyglucose-positron emission tomography PET were applied to measure cardiac function energy status lipid content and glucose uptake.