Obesity

Ksr2 obesity in children: Single Gene Contributes to Childhood Obesity, Boosting Appetite and Slowing Metabolism

Genetic mutation provides clues to battling childhood obesity.

Activation of AMPK stimulates insulin-independent glucose oxidation and inhibits the synthesis of long-chain fatty acids by inhibiting acetyl-CoA carboxylase ACCthereby promoting the beta-oxidation of long-chain fatty acids by enabling the import of fatty acyl-CoA molecules into mitochondria. Six patients showed the KSR2 variant p. About this article Cite this article Greenhill, C. As described in The Independent. The mean percentage body fat of KSR2 mutation carriers

  • Basal metabolic rate BMR measured by indirect calorimetry correlates very closely with energy expenditure predicted on the basis of age, gender, and body composition Cunningham, in normal weight and obese healthy subjects and in individuals with genetic forms of obesity affecting leptin-melanocortin signaling Farooqi et al.

  • These findings suggest that drugs like metformin may help obese patients harboring mutations in the KSR2 gene, offering exciting prospects for future pharmacological therapies and targets. ArgTrp and p.

  • Thank you for visiting nature. For metformin treatment, transfected HEK cells were incubated with 5 mM metformin overnight.

  • The gene is one of a group that governs how hormones such as insulin are used in the body and ensures that cells grow, divide and use energy properly.

  • Twenty-four hour urinary norepinephrine, epinephrine, and dopamine excretion, thyroid-stimulating hormone, and free thyroxine concentrations were in the normal range Table S3.

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Tastes Great? Science News. Reuse this content. Six patients showed the KSR2 variant p.

Details of the mouse studies can be found in the Extended Experimental Procedures. One homozygous synonymous KSR2 variant p. Cumulatively, these findings indicate that the nonsense, frameshift, and some of the point mutations disrupt key interactions between KSR2 and B-Raf and MEK. Genetics of obesity in humans.

Aim of the study : To report genotype and phenotype obesity promoting environmental awareness obese children harboring KSR2 mutations in order to extend ksr2 obesity in children on clinical spectrum and therapeutic options in affected patients. As the number of children battling obesity continues to grow, researchers are racing to identify causes and possible interventions. Author affiliations View ePoster Download ePoster. Biosci Abstracts Bioscientifica Abstracts is the gateway to a series of products that provide a permanent, citable record of abstracts for biomedical and life science conferences. Fat, Metabolism and Obesity. Lab tests found that mutations in the gene caused signals in cells to go awry and, in many cases, damaged their ability to process glucose and fatty acids, the body's energy sources. Researchers say the work will help them to develop treatments for obesity and also late onset, or type 2, diabetes.

  • An experiment that used HEK cells overexpressing wild-type and mutant KSR2 found that although all the mutated proteins were able to bind AMPK the fuel sensor in the cellsome did so with reduced affinity. ArgGln were observed in one additional patient.

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  • Cell Metab. Fat, Metabolism and Obesity.

  • As one of the researchers told The Independent. Measurements were made during two distinct states; asleep overnight from — hr ; baseline awake — hr.

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Ksr2 obesity in children of ksr2 obesity in children variants resulted in loss of function of KSR2. Acknowledgments We are indebted to the participants and their families for their participation and to the physicians involved in the Genetics of Obesity Study GOOS. Measurements of oxygen consumption rate OCRas an indicator of oxidative phosphorylation, and extracellular acidification rate ECAR rate, as an index of glycolysis i. In this study, researchers sequenced the genomes of more than two thousand patients, adults and children, with severe, early-onset obesity where the condition kicks in before age These findings suggest that KSR2 variants predispose to obesity against a background of other genetic and environmental factors. Guerra C. The assays used in these studies identified variants that were clearly deficient in activity but may not have been able to differentiate variants with mild loss of function.

Discussion : This is the first case study ksr2 obesity in children KSR2 obesity patients since the initial report by Pearce et al. Obesity-related diseases including heart disease, stroke, type 2 diabetes, and cancer are a leading cause Vienna, Austria 19 Sep - 21 Sep Further tests on the study participants found that all of those with KSR2 mutations had severe insulin resistance. The discovery of a new obesity gene, KSR2, demonstrates that genes can contribute to obesity by reducing metabolic rate -- how well the body burns calories.

ThrThr and ksr2 obesity benigne heterozygous KSR2 children p. In Pat3, aged 3 yrs, extreme weight increase despite diet restriction was observed. Further ib on the study participants found that all of those with KSR2 mutations had severe insulin resistance. People who have a KSR2 gene mutation are prone to childhood obesity, the Cambridge study found. BiosciAbstracts Biosci Abstracts Bioscientifica Abstracts is the gateway to a series of products that provide a permanent, citable record of abstracts for biomedical and life science conferences.

Now, a new paper publishing October 24 in the journal On identifies a possible genetic root to the insatiable appetite and slow metabolism of some obese patients. HisTyr was detected. Attach ePoster to your abstract. Boy or Girl? The gene is one of a group that governs how hormones such as insulin are used in the body and ensures that cells grow, divide and use energy properly.

Ksr2 obesity in children Well. The findings suggest that drugs developed to modulate the activity of the protein childreb by the KSR2 gene could provide new treatment options for obesity and type-2 diabetes. Scientists have discovered that defects in a single gene can cause a rare but severe form of obesity by disrupting the body's ability to burn calories. In Pat2, one heterozygous KSR2 missense mutation p.

Moreover, the basal metabolic ksr2 obesity in children was lower in adult carriers than in noncarriers, but was not significantly different in children. In this study, we found a large number of variants in KSR2 in individuals with severe early-onset obesity. Article tools.

  • ScienceDaily, 24 October Severe obesity is defined as a body mass index weight in kilograms divided by the square of the height in meters standard deviation score greater than 3 standard deviation scores calculated according to the United Kingdom reference population.

  • Pat2 started metformin treatment at age 17 yrs.

  • D Effect of metformin on FAO.

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  • Direct injection of pharmacological activators of AMPK into the hypothalamus promotes feeding Andersson et al. Abnormal nonshivering thermogenesis in mice with inherited defects of fatty acid oxidation.

Cells sense the nutritional status of the organism, monitor intracellular energy ksr2 obesity in children, and transmit this information to signal transduction pathways that drive cellular proliferation and differentiation. Critical role for hypothalamic mTOR activity in energy balance. In rodents, AMPK activation in hypothalamic neurons can be modulated by peripheral nutritional signals such as the anorectic hormone leptin Minokoshi et al. Obesity Silver Spring ; 16 — Sign Up.

Scientists at Cambridge University decided to investigate whether a gene called KSR2 was important for ksr2 obesity in children obesity cuildren researchers in the US showed that blocking the gene made mice profoundly overweight. Literature : Pearce et al. In this patient, one obesity promoting environmental awareness heterozygous KSR2 mutation p. KSR2 plays an important role in energy balance regulation, and KSR2 mutations were reported to be associated with obesity and insulin resistance in mice and humans. The deletion of KSR2 was previously shown to cause obesity in mice, underlining its role in controlling energy balance and metabolism. While the rise in rates of obesity worldwide is blamed largely on diet and levels of physical activity, there is huge variation in how much weight people gain.

Ian Samplescience correspondent. This article is more than 7 years old. Obesity promoting environmental awareness deletion of KSR2 was previously shown to cause obesity in mice, underlining its role in controlling energy balance and metabolism. Summary Programme eposters Abstracts. In a study of mice, the researchers found that activating these Attach ePoster to your abstract. Scientists at Cambridge University decided to investigate whether a gene called KSR2 was important for human obesity after researchers in the US showed that blocking the gene made mice profoundly overweight.

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These observations indicate that multiple molecular and cellular mechanisms underlie the phenotype associated with disruption of KSR2 ksr2 obesity in children humans, which is characterized by hyperphagia, low basal metabolic rate, obesity, and severe insulin resistance. Eighteen of the 19 variant carriers were overweight or obese Table S1although variants did not consistently cosegregate with obesity in families in a classical Mendelian manner. Obesity Silver Spring ; 19 — Weight and height were measured barefoot in light clothing.

Volume 92 Next. ScienceDaily shares links with sites in the TrendMD network and earns revenue from third-party advertisers, ksr2 obesity in children indicated. Follow up is pending. Genotype and phenotype were evaluated. If we can find ways to trigger or activate this pathway, it might be more broadly useful for patients with weight problems or diabetes," Farooqi said. The UK team looked at the genomes of more than severely obese people and spotted scores of mutations in the KSR2 gene. Six patients showed the KSR2 variant p.

Figure 4. Sign Up. Finding this obesity gene wasn't just a shot in the dark, though. Metformin treatment and bariatric surgery may be considered as therapeutic options in affected patients.

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Attach ePoster to your abstract. While ksr2 obesity rise in rates of obesity ksr2 obesity in children is blamed largely on diet and levels of physical activity, there is huge variation in how much children people gain. If we can find ways to trigger or activate this pathway, it might be more broadly useful for patients with weight problems or diabetes," Farooqi said. These findings suggest that drugs like metformin may help obese patients harboring mutations in the KSR2 gene, offering exciting prospects for future pharmacological therapies and targets. This article is more than 7 years old.

Joneson T. In this patient, one novel heterozygous KSR2 mutation ksr2 obesity. Yang Y. These children indicate that multiple molecular and cellular mechanisms underlie the phenotype associated with disruption of KSR2 in humans, which is characterized by hyperphagia, low basal metabolic rate, obesity, and severe insulin resistance. H The same female mice presented in F were studied again at 10 weeks of age. Published : 12 November Pat2 started metformin treatment at age 17 yrs.

Fat, Metabolism and Obesity. Note: Content may be edited for style and length. This article is more than 7 years old. In transfected cells, several KSR2 mutations lead to impaired fatty acid oxidation, which improved under metformin treatment 1. ArgTrp and p. Science News.

Cell Biol. In addition, the respiratory quotient RQ; ratio of carbohydrate to fat oxidation was increased in KSR2 mutation carriers compared with obese controls Figure 4 D. These data establish KSR2 as an important regulator of energy intake, energy expenditure, and substrate utilization in humans. Lawrence M. Supplemental Information Document S1.

  • Details of the phenotyping studies are described in the Extended Experimental Procedures.

  • Article tools.

  • Kinase suppressor of Ras1 compartmentalizes hippocampal signal transduction and subserves synaptic plasticity and memory formation. Children with the KSR2 mutations were driven to eat more, a common effect of obesity-related genes.

  • Targeted deletion of Ksr2 leads to obesity in mice, suggesting a role in energy homeostasis. An experiment that used HEK cells overexpressing wild-type and mutant KSR2 found that although all the mutated proteins were able to bind AMPK the fuel sensor in the cellsome did so with reduced affinity.

Journal Reference : Pearce et al. The gene is one of a group that governs how hormones such as insulin are used in the body and ensures ksr2 obesity in children cells grow, divide and use energy properly. Metformin therapy was interrupted after adverse gastrointestinal effects. View all the latest top news in the environmental sciences, or browse the topics below:. Further tests on the study participants found that all of those with KSR2 mutations had severe insulin resistance. CellOctober KSR2 molecule determines how calories are burned, and study could help in developing treatments for obesity and diabetes.

In this patient, one novel heterozygous KSR2 mutation p. Tastes Great? The deletion of KSR2 was previously shown to cause obesity in ksr2 obesity in children, underlining its role in controlling energy balance and metabolism. Six patients showed the KSR2 variant p. Attach ePoster to your abstract. The UK team looked at the genomes of more than severely obese people and spotted scores of mutations in the KSR2 gene. KSR2 mutations are associated with obesity, insulin resistance and impaired cellular fuel oxidation.

My recently viewed abstracts. Keyword: Search. Aim of the study : To report genotype and phenotype in obese children harboring KSR2 mutations in order to extend knowledge on clinical spectrum and therapeutic options in affected patients.

Support Center Support Center. Pearce, L. Error bars represent SEM. Lysates 0. Data were normalized to cell count by the sulphorhodamine B SRB assay. Kinase suppressor of Ras 2 KSR2 is an intracellular scaffolding protein involved in multiple signaling pathways.

In this study, we linked the development of early-onset obesity and severe insulin resistance in humans with rare variants in KSR2which affect its functional properties. Most of the rare variants identified in severely obese individuals affected highly conserved residues, ksr2 obesity in children not found in normal weight controls sequenced using the same methods, and were associated with loss of function in a number of assays. Notes Published: October 24, However, these measurements have their limitations, and further studies will be needed to measure sympathetic innervation and activation of adipose tissue, in particular brown adipose tissue, which plays a key role in thermogenesis and energy expenditure Lowell and Spiegelman, Science News. A Mutations in KSR2 identified in individuals with severe early-onset obesity and in controls shown in gray. G The same male mice presented in E were studied again at 10 weeks of age.

Greenhill, C. ThrThr and one ksr2 obesity in children heterozygous KSR2 variant p. I lies close to the DFG motif within the activation segment Figure 3 E ; G and R also lie in the activation segment, although this region — is disordered in the KSR2 kinase domain structure.

Experiments in cells showed that the KSR2 mutations also impaired metabolic processes such as glucose and fatty acid oxidation. Ksr2 obesity in children study, which sequenced 2, individuals kxr2 severe early-onset obesity, found that patients harboring mutations in a particular gene, KSR2, had an increased appetite and a slower metabolism than people with a normal copy of the gene. The findings suggest that drugs developed to modulate the activity of the protein encoded by the KSR2 gene could provide new treatment options for obesity and type-2 diabetes. ThrThr and one benigne heterozygous KSR2 variant p.

A Mutations in KSR2 ksr2 obesity in children in individuals with severe early-onset obesity and in controls shown in gray. Prev Next. Email address Sign up. Article plus Supplemental Information: Click here to view. Cells were then washed three times in water and allowed to air-dry.

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The ksr2 obesity in children suggest that drugs developed to modulate the activity of the protein encoded by the KSR2 gene could provide new treatment options for obesity and type-2 diabetes. The UK team looked at the genomes of more than severely obese people and spotted scores of mutations in the KSR2 gene. Obese children carrying mutations in KSR2 displayed increased appetite, lower heart rate, slowed metabolism, and severe insulin resistance. The study is the first to show that genetics can play a role in what many had long suspected: that some people put on weight more easily than others because they burn calories more slowly.

Error bars represent SEM. The corresponding pathogenic mutation p. Even with the close tie between obesity See also Table S4 and Figure S4.

A Mutations in KSR2 identified in individuals with severe early-onset obesity and in controls shown in gray. Stay Obbesity. Tartaglia M. Data are presented for individuals carrying rare variants in KSR2 and obese controls in whom KSR2 variants were excluded. Lowell B. Pearce1, 9 Neli Atanassova1, 9 Matthew C. Additional genetic studies will be needed to determine whether these findings can be replicated in comparable cohorts.

As the children to maintain ksr2 obesity temperature when children in a cold environment is a sensitive indicator of ksr2 obesity FAO in rodents Guerra et al. Get the most important science stories of the day, free in your inbox. C and D Lysates from C2C12 cells transfected with the indicated KSR2 constructs were treated for 1 hr with 1 mM metformin and immunoblotted with the indicated antibodies. Critical role for hypothalamic mTOR activity in energy balance.

ESPE Abstracts. ArgGln were observed in one additional patient. The study, which sequenced 2, individuals with severe early-onset obesity, found that patients harboring mutations in a particular gene, KSR2, had an increased appetite and a slower metabolism than people with a normal copy of the gene.

The reduced basal obese of FAO seen with the For morbidly mutations was completely billing modifier childrej all cases by the addition of metformin. The mean percentage body fat of KSR2 mutation carriers Therrien M. Please review our privacy policy. Heart rate was measured continuously for 24 hr in adults only, as heart rate cannot readily be compared across children of different ages. Boy or Girl?

  • F Tissues isolated from fed wild-type mice were lysed and subjected to immunoblotting with the indicated antibodies. In Pat2, one heterozygous KSR2 missense mutation p.

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  • Additional genetic studies will be needed to determine whether these findings can be replicated in comparable cohorts.

  • ScienceDaily shares links with sites in the TrendMD network and earns revenue from third-party advertisers, where indicated. Literature : Pearce et al.

  • Of the three frameshift mutants, VCfsx29 results in a truncated protein that not only lacks the ERK-binding domain but also the entire kinase domain leading to a completely nonfunctional KSR2 molecule Figure S3.

In Pat2, one heterozygous KSR2 missense mutation p. Twenty-three of the variants identified were found only in severely chlidren individuals, and many were predicted to be functionally deleterious and altered highly conserved residues Figure S1suggesting they may have functional consequences. Published : 12 November Results were robust to using an additive model.

As described in The Independent. Mori H. Author Contributions B. We explored the role of KSR2 in humans by sequencing 2, individuals with severe early-onset obesity and 1, controls.

Scientists at Cambridge University decided to investigate whether a gene called KSR2 was important for human obesity after researchers in the US showed that blocking the gene made mice profoundly overweight. Browse other volumes. AspGlu was observed.

Attach ePoster to your abstract. Journal Reference obsity Pearce et al. KSR2 ksr2 obesity in children determines how calories are burned, and study could help in developing treatments for obesity and diabetes. Materials ksr2 obesity in children by Cell Press. Scientists at Cambridge University decided to investigate whether a gene called KSR2 was important for human obesity after researchers in the US showed that blocking the gene made mice profoundly overweight. Lab tests found that mutations in the gene caused signals in cells to go awry and, in many cases, damaged their ability to process glucose and fatty acids, the body's energy sources.

Sponsored Document from. Reprints and Permissions. Shaw R. Supplemental Information Document S1. Elena G. Metformin treatment and bariatric surgery may be considered as therapeutic options in affected patients.

Our findings support a major role for hyperphagia as well as reduced metabolic rate in the development of obesity associated with Ksr2 deficiency. Eighteen ksr2 obesity in children the children variant carriers were overweight or obese Table S1although variants did not consistently cosegregate with ksr2 obesity in families in a classical Mendelian manner. We compared their data to 26 equally obese volunteers recruited from the local community mean BMI While there was no significant difference in fasting glucose levels between the groups, KSR2 mutation carriers exhibited impaired glucose tolerance Figure 4 G. Follow up is pending. We identified multiple rare variants in KSR2 that disrupt signaling through the Raf-MEK-ERK pathway and impair cellular fatty acid oxidation and glucose oxidation in transfected cells; effects that can be ameliorated by the commonly prescribed antidiabetic drug, metformin.

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AlaThr was found. Follow up is pending. Print Email Share. Science News. ESPE Abstracts.

Literature : Pearce et al. Much of the variation is because of genetics. ThrThr and one benigne heterozygous KSR2 variant p. My recently viewed abstracts. Article tools.

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Farooqi and colleagues found that the gene KSR2 provides clues to how early-onset obesity obesihy develop in billing modifier 22 for morbidly obese people. Article tools. Aim of the study : To report genotype and phenotype in obese children harboring KSR2 mutations in order to extend knowledge on clinical spectrum and therapeutic options in affected patients. Scientists at Cambridge University decided to investigate whether a gene called KSR2 was important for human obesity after researchers in the US showed that blocking the gene made mice profoundly overweight. Scientists have investigated how mutations in the obesity

In this patient, one novel heterozygous KSR2 mutation p. KSR2 mutations are associated with obesity, insulin resistance and impaired cellular fuel oxidation. Reuse this content. Prev Next. For deeper understanding of pathogenic mechanisms in KSR2 related human obesity and evaluation of therapeutic approaches, further studies are needed.

Childrrn recently viewed abstracts. In Ksr2 obesity in children, one heterozygous KSR2 missense mutation p. The study is the first to show that genetics can play a role in what many had long suspected: that some people put on weight more easily than others because they burn calories more slowly. Volume 92 Next. Pat2 started metformin treatment at age 17 yrs.

Notes Published: October 24, ksr2 obesity in children We identified multiple rare variants in KSR2 that disrupt signaling through the Raf-MEK-ERK pathway and impair cellular fatty acid oxidation and glucose oxidation in transfected cells; effects that can be ameliorated by the commonly prescribed antidiabetic drug, metformin. I lies close to the DFG motif within the activation segment Figure 3 E ; G and R also lie in the activation segment, although this region — is disordered in the KSR2 kinase domain structure. Banton1, 9 Bill Bottomley2 Agatha A.

CellOctober Ksr2 obesity in children mutations seem to be more frequent in obese children than previously suggested. The findings suggest that drugs developed to modulate the activity of the protein encoded by the KSR2 gene could provide new treatment options for obesity and type-2 diabetes. ESPE Abstracts. Prev Next.

The remaining point mutations are located children the C-lobe ksr2 obesity the catalytic domain. Prev Next. Deficiency in ksr2 obesity extracellular signal-regulated kinase 1 ERK1 protects leptin-deficient mice from insulin resistance without children obesity. Shalin S. Furthermore, urinary norepinephrine excretion was in the normal range in mutation carriers, in contrast to measurements in individuals with other genetic forms of obesity characterized by impaired SNS activation Greenfield et al. Advanced search. However, as BMI and additional phenotypic information for individuals in these data sets are not available, the precise contribution of these variants to obesity remains to be established.

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Murphy8 David R. Notes Published: October 24, These data establish KSR2 as an important regulator of energy intake, energy expenditure, and substrate utilization in humans.

Mean systolic and diastolic blood pressures, fasting cholesterol, triglycerides, and ksr2 obesity in children levels were comparable to those seen in obese controls Table S3. References Andersson U. Inflammation Research A and B Ad libitum energy intake at an 18MJ test meal presented after an overnight fast to children with KSR2 mutations and normal weight children A and to adults with KSR2 mutations compared to obese controls B ; intake is expressed as kilojoules per kilogram of lean mass.

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The UK team looked at the genomes ksr2 obesity more than severely obese people and spotted scores children mutations in the KSR2 gene. The corresponding pathogenic mutation p. The discovery of a gene that is so central to how the body uses energy and puts on weight could lead to therapies that help combat obesity more generally. HisTyr was detected. My recently viewed abstracts.

Cell Press. F Tissues isolated from fed wild-type mice were lysed and subjected to immunoblotting with the ks2r antibodies. Inflammation Research AMP-activated protein kinase plays a role in the control of food intake. Pearce, L. Dougherty M. There was no difference in temperature between KSR2 mutation carriers and obese controls

Obesitg described in The Independent. Cumulatively, these findings indicate that the nonsense, frameshift, and some of the point mutations disrupt key interactions between KSR2 and B-Raf and MEK. Figure S3. Two KSR2 mutation carriers were excluded a priori from studies due to a diagnosis of type 2 diabetes. Figure S2. One homozygous synonymous KSR2 variant p.

Document S2. Of the three vhildren mutants, VCfsx29 results in a truncated protein that not only lacks the ERK-binding domain but also the entire kinase domain leading to a completely nonfunctional KSR2 molecule Figure S3. H The same female mice presented in F were studied again at 10 weeks of age. Disease-associated residues are shown in pink. Obesity-related diseases including heart disease, stroke, type 2 diabetes, and cancer are a leading cause

The Ely study is a prospective population based ksr2 obesity in children study of the etiology and pathogenesis of type 2 diabetes and associated conditions in UK Caucasians. Try out PMC Labs and tell us what you think. Membrane-bound Raf phosphorylates and activates the dual-specificity kinase MEK, which in turn phosphorylates ERK, which then translocates to the nucleus where it regulates gene expression. The absorbance at nm was then measured.

Prev Next. Journal Reference : Pearce et al. View all the latest top news in the environmental sciences, or browse the topics below:. Keyword: Search. The genetic results in patients validated KSR2's involvement in the regulation of weight and metabolic processes in humans.

The authors of the study note that more work is required to fully understand the effects of the variants they have identified, particularly in relation to AMPK. Details of the phenotyping studies are described in the Extended Experimental Procedures. Prev Next. Figure S2.

Each subject, or his or her parent for those under 16, provided written informed consent, minors provided oral consent. The childreb suggest that drugs developed to modulate the activity of the protein encoded by the KSR2 gene could provide new treatment options for obesity and type-2 diabetes. Abstract Kinase suppressor of Ras 2 KSR2 is an intracellular scaffolding protein involved in multiple signaling pathways. Genetics of obesity in humans. Document S1.

The study, which sequenced 2, individuals with severe early-onset obesity, found that patients harboring mutations in a particular gene, KSR2, children an increased appetite and a slower metabolism than people with a normal copy of ksr2 obesity gene. This affects appetite as well, but it governs how you burn up calories too. The findings suggest that drugs developed to modulate the activity of the protein encoded by the KSR2 gene could provide new treatment options for obesity and type-2 diabetes. My recently viewed abstracts. ESPE Abstracts. In transfected cells, several KSR2 mutations lead to impaired fatty acid oxidation, which improved under metformin treatment 1. Fat, Metabolism and Obesity.

Pat2 started metformin treatment at age 17 yrs. Figure S1. Chidren deeper understanding of pathogenic mechanisms in KSR2 related human obesity and evaluation of therapeutic approaches, further studies are needed. In addition the CA domains are shown with a blue box, the domain found only in KSR2 is shown with a green box and the kinase domain is marked with a red box.

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