Genetics of adult body mass and maintenance of adult body mass in captive baboons (Papio hamadryas subspecies)

Jaquish, Cashell E.; Dyer, Tom; Williams‐Blangero, Sarah; Dyke, Bennett; Leland, M. Michelle; Blangero, John

doi:10.1002/(sici)1098-2345(1997)42:4<281::aid-ajp3>3.0.co;2-t

Cited by 10 publications

(7 citation statements)

References 13 publications

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“…This study suggests that obesity phenotypes associated with insulin resistance in baboons are heritable, as in humans. A large genetic component to variation in weight was found in the present study (80%); this value is higher than the 50% previously reported for the same colony (31). Presumably, the greater percentage is due to the use of two subspecies in the present study, as opposed to six in the study by Jaquish et al (31).…”

Section: Discussioncontrasting

confidence: 90%

“…A large genetic component to variation in weight was found in the present study (80%); this value is higher than the 50% previously reported for the same colony (31). Presumably, the greater percentage is due to the use of two subspecies in the present study, as opposed to six in the study by Jaquish et al (31). The large h 2 of weight in baboons as compared with humans (32) might be due to the reduced environment effect in the animal model, given that the animals share the same diet and living conditions.…”

Section: Discussioncontrasting

confidence: 90%

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Pleiotropic Effects of Genes for Insulin Resistance on Adiposity in Baboons

et al. 2004

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Objective: Previous research has suggested a genetic contribution to the development of insulin resistance and obesity. We hypothesized that the same genes influencing insulin resistance might also contribute to the variation in adiposity. Research Methods and Procedures:A total of 601 (200 male, 401 female) adult baboons (Papio hamadryas) from nine families with pedigrees ranging in size from 43 to 121 were used in this study. Plasma insulin, glucose, C-peptide, and adiponectin were analyzed, and homeostasis model assessment of insulin resistance (HOMA IR) was calculated. Fat biopsies were collected from omental fat tissue, and triglyceride concentration per gram of fat tissue was determined. Body weight and length were measured, and BMI was derived. Univariate and bivariate quantitative genetic analyses were performed using SOLAR. Results: Insulin, glucose, C-peptide, and adiponectin levels, HOMA IR, triglyceride concentration of fat tissue, body weight, and BMI were all found to be significantly heritable, with heritabilities ranging from 0.15 to 0.80. Positive genetic correlations (r G s) were observed for HOMA IR with C-peptide (r G ϭ 0.88 Ϯ 0.10, p ϭ 0.01), triglyceride concentration in fat tissue (r G ϭ 0.86 Ϯ 0.33, p ϭ 0.02), weight (r G ϭ 0.50 Ϯ 0.20, p ϭ 0.03), and BMI (r G ϭ 0.64 Ϯ 0.22, p ϭ 0.02). Discussion: These results suggest that a set of genes contributing to insulin resistance also influence general and central adiposity phenotypes. Further genetic research in a larger sample size is needed to identify the common genes that constitute the genetic basis for the development of insulin resistance and obesity.

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Section: Discussioncontrasting

confidence: 90%

Section: Discussioncontrasting

confidence: 90%

Pleiotropic Effects of Genes for Insulin Resistance on Adiposity in Baboons

et al. 2004

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“…Along with studies utilizing NHPs to investigate the physiological and metabolic processes underlying obesity and its associated endophenotypes, studies using NHPs have also provided important insights into the genetic and epigenetic factors that also contribute to the risk for developing obesity (Cai et al 2004;Schwartz 1989;Tejero et al 2004aTejero et al , 2004bVoruganti et al 2007Voruganti et al , 2008. For example, Jaquish and colleagues (Jaquish et al 1997) reported a genetic contribution accounting for 51% of the total variance in mean adult body weight and 12% of the variance in body weight stability in baboons, demonstrating a substantial genetic component to variations of body weight in these animals, a finding consistent with what has been reported in numerous studies of the genetics of obesity in humans. Additional work in baboons found significant additive genetic heritabilities for serum leptin levels (h 2 = 0.21), weight (h 2 = 0.62), fat mass (h 2 = 0.41), fat free mass (h 2 = 0.32), and the ratio of fat free mass (h 2 = 0.84) (Comuzzie et al 2003).…”

Section: Obesitymentioning

confidence: 99%

Use and Importance of Nonhuman Primates in Metabolic Disease Research: Current State of the Field

et al. 2017

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Obesity and its multiple metabolic sequelae, including type 2 diabetes, cardiovascular disease, and fatty liver disease, are becoming increasingly widespread in both the developed and developing world. There is an urgent need to identify new approaches for the prevention and treatment of these costly and prevalent metabolic conditions. Accomplishing this will require the use of appropriate animal models for preclinical and translational investigations in metabolic disease research. Although studies in rodent models are often useful for target/pathway identification and testing hypotheses, there are important differences in metabolic physiology between rodents and primates, and experimental findings in rodent models have often failed to be successfully translated into new, clinically useful therapeutic modalities in humans. Nonhuman primates represent a valuable and physiologically relevant model that serve as a critical translational bridge between basic studies performed in rodent models and clinical studies in humans. The purpose of this review is to evaluate the evidence, including a number of specific examples, in support of the use of nonhuman primate models in metabolic disease research, as well as some of the disadvantages and limitations involved in the use of nonhuman primates. The evidence taken as a whole indicates that nonhuman primates are and will remain an indispensable resource for evaluating the efficacy and safety of novel therapeutic strategies targeting clinically important metabolic diseases, including dyslipidemia and atherosclerosis, type 2 diabetes, hepatic steatosis, steatohepatitis, and hepatic fibrosis, and potentially the cognitive decline and dementia associated with metabolic dysfunction, prior to taking these therapies into clinical trials in humans.

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“…To further evaluate the utility of the visual BCS system, we apply animal models to estimate BCS heritability in our population. As BCSs represent body condition, we expect the narrow sense heritability (i.e., the fraction of phenotypic variance that can be attributed to variation in the additive effects of genes) to be in the range of previously reported primate body condition measures (h 2 varies from 0.40 to 0.80) (Cai et al, 2004;Comuzzie et al, 2003;Jaquish et al, 1997;Joganic et al, 2018;Kavanagh et al, 2007;Kimock et al, 2019;Schmitt et al, 2018). Next, we set out to investigate which additional factors explain variation in BCSs, such as sex, age, obesity-related diseases, and caloric content of the diet.…”

Section: Introductionmentioning

confidence: 99%

Visually assessed body condition shows high heritability in a pedigreed great ape population

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Eens

Laméris

et al. 2023

American J Primatol

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Body condition, a measure for relative fat mass, is associated with primate health, fitness, and overall welfare. Body condition is often influenced by dietary factors, age, and/or sex, but several body condition measures (body weight, weight‐to‐height ratios, and so on) also show high heritability across primate species, indicating a role of genetic effects. Although different measures for body condition exist, many require direct handling of animals, which is invasive, time‐consuming, and expensive, making them impractical in wild and captive settings. Therefore, noninvasive visual body condition score (BCS) systems were developed for various animal species, including macaques and chimpanzees, to visually assess relative fat mass. Here we evaluate the utility of a visual BCS system in bonobos by assessing (1) inter‐rater reliability, (2) links with body mass, a traditional hands‐on measure of condition, and (3) the factors driving individual variation in BCS. We adapted the chimpanzee BCS system to rate 76 bonobos in 11 European zoos (92% of the adult population). Inter‐rater reliability was high (s* = 0.948), BCSs were positively associated with body mass (β = 0.075) and not predicted by diet, sex, or age, nor were they associated with a higher abundance of obesity‐related diseases. Instead, BCSs showed high levels of heritability (h2 = 0.637), indicating that a majority of body condition variation in bonobos is attributable to genetic similarity of the individuals. This is in line with reported h2‐values for traditional body condition measures in primates and provides support for the reliability of visual BCS systems in great apes. The results of this study emphasize an often unanticipated role of genetics in determining primate body fat and health that has implications for the management of captive primates. Application of this tool in wild populations would aid to unravel environmental from genetic drivers of body condition variation in primates.

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Genetics of adult body mass and maintenance of adult body mass in captive baboons (Papio hamadryas subspecies)

Cited by 10 publications

References 13 publications

Pleiotropic Effects of Genes for Insulin Resistance on Adiposity in Baboons

Pleiotropic Effects of Genes for Insulin Resistance on Adiposity in Baboons

Use and Importance of Nonhuman Primates in Metabolic Disease Research: Current State of the Field

Visually assessed body condition shows high heritability in a pedigreed great ape population

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