Metabolic differences between obesity-prone and obesity-resistant rats

Chang, Sam K. C.; Bs, Graham; Yakubu, F.; Lin, Ding; Peters, J. C.; Hill, James O.

doi:10.1152/ajpregu.1990.259.6.r1103

Cited by 122 publications

(139 citation statements)

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“…Supporting this suggestion, individual variation in basal fat oxidation rates are a consistent predictor of predisposition to obesity in both humans [70][71][72][73][74][75][76] and animals. 77,78 The common point in these two scenarios is that they do not rely on any assumption that obesity was historically advantageous. Rather they make the opposite assumption that genes predisposing to obesity were NOT under any positive selection.…”

Section: An Alternative Perspective: 'Drifty' Genesmentioning

confidence: 99%

Thrifty genes for obesity, an attractive but flawed idea, and an alternative perspective: the ‘drifty gene’ hypothesis

2008

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Almost 50 years ago Neel proposed a hypothesis to explain the prevalence of obesity and diabetes in modern societyFthe 'thrifty gene' hypothesis. The fundamental basis of the hypothesis was that, in our early evolutionary history, genes, that promoted efficient fat deposition would have been advantageous because they allowed their holders to survive at periods of famine. In modern society, such genes are disadvantageous because they promote fat deposition in preparation for a famine that never comes, and the result is widespread obesity and diabetes. In recent years I, and others, have questioned some of the fundamental assumptions of this hypothesisFparticularly focusing on whether differential survival of lean against obese in famines provides sufficient selective pressure for the spread of so-called 'thrifty genes'. These arguments have been criticized because famines not only affect survival but also fecundity, and obese people would be expected to sustain fecundity longer in the face of food shortages. In this paper, I show that the reduced fecundity argument is flawed because famines are almost universally followed by periods of enhanced fecundity, which offsets the decline observed during the famine itself. The net effect of famines on fecundity is consequently insufficient to rescue the thrifty gene idea. Elsewhere, I have suggested an alternative scenario that subsections of the population have a genetic predisposition to obesity due to an absence of selection, combined with genetic drift. The scenario presented earlier was based on evidence from prehistory concerning the release of our ancestors from heavy predation pressure around 2 million years ago. I suggest here that this is one of a number of potential scenarios based on random genetic drift that may explain the specific aetiology of the obesity epidemic. Together, these alternatives, based on central notion that genetic drift rather than positive selection was a dominant factor, may be called the 'drifty gene' hypothesis.

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Section: An Alternative Perspective: 'Drifty' Genesmentioning

confidence: 99%

Thrifty genes for obesity, an attractive but flawed idea, and an alternative perspective: the ‘drifty gene’ hypothesis

2008

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“…However, the role of RMR in the susceptibility to obesity is controversial because obesity is usually associated with high absolute metabolic rate (Leibel et al, 1995;Ravussin and Gautier, 1999). The ability to avoid dietary obesity produced by a high-fat diet may also be related with high rates of fat oxidation (Chang et al, 1990). In this sense, Zurlo et al (1990) found that low-fat oxidizers exhibited a higher risk of gaining weight in comparison to high-fat oxidizers, whereas Thomas et al (1992) reported an increase in fat oxidation in lean but not in obese subjects 7 days after switching to a high-fat diet.…”

Section: Introductionmentioning

confidence: 99%

Differences in short-term metabolic responses to a lipid load in lean (resistant) vs obese (susceptible) young male subjects with habitual high-fat consumption

2006

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Objective: To determine the role of macronutrients oxidation ability in the postprandial response to a high lipid load in the mechanisms conferring resistance or susceptibility to obesity. Subjects and design: Nine lean and nine obese young male subjects with habitual similar high-fat intake (440 % of energy) and comparable physical activity were selected and categorized as 'resistant', those who remained lean (body mass index (BMI) o25 kg/m 2 ), and 'susceptible', those who were obese (BMI430 kg/m 2 ). Fasting blood samples were taken for the evaluation of blood metabolic and hormonal variables. Resting metabolic rate (RMR) and substrates oxidation were measured by indirect calorimetry, in the fasting state and every 30 min for 3 h after a rich lipid meal (fat 94.7%) supplied to cover the 50% of the volunteers energy requirements. The study was performed at the Metabolic Unit of the University of Navarra. Results: Fasting RMR and lipid oxidation were higher in obese-susceptible subjects. However, similar values were found in both groups after adjustment for fat mass and free fat mass. The cumulative postprandial fat oxidation was also similar in both groups (despite having different tissue metabolic activity), whereas cumulative carbohydrate oxidation was lower in the obesesusceptible group. The thermic effect of food (% of dietary induced thermogenesis) was lower (Po0.05) in the susceptibleobese subjects. The energy and fat balance were more positive in the obesity-susceptible individuals after the high fat load, who also showed higher fasting homeostatic model assessment index, low-density lipoprotein-cholesterol and triacylglyceride levels, hyperleptinemia and hypoadiponectinemia. Conclusion: Lean-resistant individuals came closer to achieving fat balance than obese-susceptible subjects. These metabolic and hormonal differences are probably genetically determined.

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“…The body mass of obesity-prone rats was significantly higher than obesity-resistant rats and low-fat-fed rats, while that of obesity-resistant rats was identical to that of low-fat fed rats. 20,21 The combination of this animal model and the two different diet compositions might thus help us to elucidate the mechanism underlying the relationships between muscle characteristics, fat accumulation and diet composition. Therefore, subjecting CR and FFDR to a low-or high-fat diet, we examined the relationship between the muscle characteristics, including the fibre type composition and the oxidative enzyme activity and body fat accumulation and also determined whether or not the composition of the diets affects such characteristics.…”

Section: Introductionmentioning

confidence: 99%

Dietary obesity-resistance and muscle oxidative enzyme activities of the fast-twitch fibre dominant rat

Suwa

Kumagai

Higaki³

et al. 2002

Int J Obes

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OBJECTIVES:To clarify whether the muscle fibre composition and=or muscle oxidative enzyme activity are related to dietary body weight gain and abdominal fat accumulation. METHODS: Genetically fast-twitch fibre dominant rats (FFDR) and control rats (CR) were divided into low-fat (20% of energy from fat) or high-fat (60% of energy from fat) diet groups: CR with a low-fat diet (CL); CR with a high-fat diet (CH); FFDR with a low-fat diet (FL); and FFDR with a high-fat diet (FH). After 6 weeks of following such diets, the body weight gain, abdominal fat content, food intake, muscle fibre composition and oxidative enzyme activities were estimated. RESULTS: The total body weight gain in CH was from 18 to 62% higher than in the other groups (P < 0.05) and percentage abdominal fat in CH was also from 26 to 61% higher than in the other groups (P < 0.05), while the energy intake did not differ among the groups. The percentage of type IIX fibres of M. gastrocnemius in FL (33.4%) and FH (36.3%) were higher than in CL (16.8%) and CH (19.8%; P < 0.05), and the type IIA fibres of M. soleus in FL (14.1%) and FH (11.8%) were higher than in CL (2.0%) and CH (3.5%; P < 0.05). The citrate synthase (CS) activity of of M. plantaris in FL and FH were higher than CL (46 and 54%, respectively, P < 0.05). b-Hydroxyacyl CoA dehydrogenase (HAD) activity in FL and FH were higher than in CL (21 and 31%, respectively, P < 0.05) and that in FH was higher than CH (23%, P < 0.05). On the other hand, the enzyme activities of M. gastrocnemius and soleus were identical among the groups. CONCLUSION: The FFDR was more obesity-resistant than the CR after a high-fat diet. These results suggest that the muscle oxidative capacity rather than muscle fibre composition is a possible determinant of obesity.

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Metabolic differences between obesity-prone and obesity-resistant rats

Cited by 122 publications

References 0 publications

Thrifty genes for obesity, an attractive but flawed idea, and an alternative perspective: the ‘drifty gene’ hypothesis

Thrifty genes for obesity, an attractive but flawed idea, and an alternative perspective: the ‘drifty gene’ hypothesis

Differences in short-term metabolic responses to a lipid load in lean (resistant) vs obese (susceptible) young male subjects with habitual high-fat consumption

Dietary obesity-resistance and muscle oxidative enzyme activities of the fast-twitch fibre dominant rat

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