The M16 Mouse: An Outbred Animal Model of Early Onset Polygenic Obesity and Diabesity

Allan, M. F.; Eisen, E. J.; Pomp, Daniel

doi:10.1038/oby.2004.176

Cited by 46 publications

(43 citation statements)

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“…Both male and female express early onset of a moderate obesity due to hyperphagia and have high levels of insulin, leptin and cholesterol. The diabetic phenotype of M16 permits research of obesity/diabetes syndrome with early onset as it recorded in human population as a current tendency [120].…”

Section: Tsumura Suzuki Obese Diabetic (Tsod) Mousementioning

confidence: 99%

Development of Improved Animal Models for the Study of Diabetes

Ciobotaru¹

2013

Diabetes Mellitus - Insights and Perspectives

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Section: Tsumura Suzuki Obese Diabetic (Tsod) Mousementioning

confidence: 99%

Development of Improved Animal Models for the Study of Diabetes

Ciobotaru¹

2013

Diabetes Mellitus - Insights and Perspectives

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“…A very large variation in phenotypes was created in the F 2 Phenotypic correlations between WT15, body composition traits and glucose in the F 2 population are presented in Table 3. As expected, WT15 is highly correlated with PAD, LIV, FAT, LEAN, and BMD.…”

Section: Phenotypic Characterization Of the M16i ϫ Mb2 F 2 Populationmentioning

confidence: 99%

“…The M16 line was the result of 27 generations of selective breeding for rapid growth rate (15), resulting in correlated responses of polygenic obesity and symptoms of type II diabetes (2). Full-sib mating within M16 has led to a fully inbred derivative denoted as M16i (21).…”

mentioning

confidence: 99%

Fine mapping of a QTL region with large effects on growth and fatness on mouse chromosome 2

Jerez-Timaure

Eisen

Pomp

2005

Physiological Genomics

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We combined the use of a congenic line and recombinant progeny testing (RPT) to characterize and fine map a previously identified region of distal mouse chromosome 2 (MMU2) harboring quantitative trait loci (QTL) with large effects on growth and fatness. The congenic line [M16i.B6-( D2Mit306- D2Mit52); MB2] was created using an inbred line (M16i) derived from a line that had undergone long-term selection for rapid weight gain (M16) as the recipient for an ∼38-cM region on MMU2 from the inbred line C57BL/6J. A large F2 cohort (1,200 mice) originating from a cross between MB2 and M16i was created, and 40 F2 males with defined recombinations within the QTL region were used to produce 665 segregating progeny. Linkage analysis of the F2 population detected QTL with very large effects on body weight, body fat, lean tissue mass, bone mineral density, and liver weight. Confidence intervals of the QTL were narrowed to regions of 1.5–4.5 cM. Analysis of progeny of the recombinant F2 males confirmed the existence of the QTL and further contributed to localization of their map positions. These efforts confirmed the presence of QTL with major effect on MMU2, narrowed the estimated region harboring the QTL from 38 to 12 cM, and further characterized phenotypic effects of the QTL, effectively culminating in a significantly decreased pool of positional candidate genes potentially representing these genes controlling predisposition to growth and fatness.

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“…As several mouse models for monogenic or polygenic obesity like NZO [43], KK [44], and M16 [45] develop diabetes at early ages, the obese BFMI860 line constitutes a unique model to identify mechanisms and causes of both obesity and eventually the development of type 2 diabetes in high-aged individuals.…”

Section: Disclosure Statementmentioning

confidence: 99%

Features of the Metabolic Syndrome in the Berlin Fat Mouse as a Model for Human Obesity

Hantschel

Wagener²,

Neuschl³

et al. 2011

Obes Facts

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Background: The Berlin Fat Mouse BFMI860 is a polygenic obesity mouse model which harbors a natural major gene defect resulting in early onset of obesity. To elucidate adult bodily responses in BFMI860 mice that develop juvenile obesity, we studied features of the metabolic syndrome at 20 weeks. Methods: We examined fat deposition patterns, adipokines, lipid profiles in serum, glucose homeostasis, and insulin sensitivity in mice that were fed either a standard maintenance (SMD) or a high-fat diet (HFD). Results: Like many obese humans, BFMI860 mice showed hyperleptinemia accompanied by hypoadiponectinemia already at SMD that was further unbalanced as a result of HFD. Furthermore, BFMI860 mice had high triglyceride concentrations. However, triglyceride clearance after an oral oil gavage was impaired on SMD but improved on HFD. The oral and intraperitoneal glucose as well as the insulin tolerance tests provided evidence for reduced insulin sensitivity under SMD and insulin resistance on HFD. BFMI860 mice can maintain normal glucose clearance over a wide range of feeding conditions according to an adaptation via increasing the insulin concentrations. Conclusions: BFMI860 mice show obesity, dyslipidemia, and insulin resistance as three major components of the metabolic syndrome. As these mice develop the described phenotype as a result of a major gene defect, they are a unique model for the investigation of genetic and pathophysiological mechanisms underlying the observed features of the metabolic syndrome and to search for potential strategies to revert the adverse effects under controlled conditions.

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The M16 Mouse: An Outbred Animal Model of Early Onset Polygenic Obesity and Diabesity

Cited by 46 publications

References 50 publications

Development of Improved Animal Models for the Study of Diabetes

Development of Improved Animal Models for the Study of Diabetes

Fine mapping of a QTL region with large effects on growth and fatness on mouse chromosome 2

Features of the Metabolic Syndrome in the Berlin Fat Mouse as a Model for Human Obesity

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