Estimation of available energy of dietary fibres by indirect calorimetry in rats

BackgroundAccording to the World Health Organization (WHO) there is a pandemic of obesity with approximately 300 million people being obese. Typically, human obesity has a polygenetic causation. Neutral endopeptidase (NEP), also known as neprilysin, is considered to be one of the key enzymes in the metabolism of many active peptide hormones.Methodology/Principal FindingsAn incidental observation in NEP-deficient mice was a late-onset excessive gain in body weight exclusively from a ubiquitous accumulation of fat tissue. In accord with polygenetic human obesity, mice were characterized by deregulation of lipid metabolism, higher blood glucose levels, with impaired glucose tolerance. The key role of NEP in determining body mass was confirmed by the use of the NEP inhibitor candoxatril in wild-type mice that increased body weight due to increased food intake. This is a peripheral and not a central NEP action on the switch for appetite control, since candoxatril cannot cross the blood-brain barrier. Furthermore, we demonstrated that inhibition of NEP in mice with cachexia delayed rapid body weight loss. Thus, lack in NEP activity, genetically or pharmacologically, leads to a gain in body fat.Conclusions/SignificanceIn the present study, we have identified NEP to be a crucial player in the development of obesity. NEP-deficient mice start to become obese under a normocaloric diet in an age of 6–7 months and thus are an ideal model for the typical human late-onset obesity. Therefore, the described obesity model is an ideal tool for research on development, molecular mechanisms, diagnosis, and therapy of the pandemic obesity.

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“…[36]. Oxygen concentration in the air was measured paramagnetically and carbon dioxide concentration by infrared absorption.…”

Section: Methodsmentioning

confidence: 99%

New Function for an Old Enzyme: NEP Deficient Mice Develop Late-Onset Obesity

et al. 2010

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“…Oxygen consumption and carbon dioxide production were measured in 6-minute intervals over 23 hours, from 9 AM to 8 AM the next day. RQ and TEE were calculated according to Aust et al 19 The mean of the 10 lowest TEE values (kilojoules per minute) was accepted to calculate resting energy expenditure (REE; kilojoules per day). The difference between TEE and REE values was used to calculate total thermogenesis (TTh; kilojoules per day), which implied postprandial thermogenesis, as well as nonexercise and exercise activity thermogenesis.…”

Section: Energy Metabolismmentioning

confidence: 99%

Energy Metabolism in Human Renin-Gene Transgenic Rats

Gratze

Boschmann²,

Dechend³

et al. 2009

Hypertension

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Abstract-Renin initiates angiotensin II formation and has no other known functions. We observed that transgenic rats (TGR) overexpressing the human renin gene (hREN) developed moderate obesity with increased body fat mass and glucose intolerance compared with nontransgenic Sprague-Dawley (SD) rats. The metabolic changes were not reversed by an angiotensin-converting enzyme inhibitor, a direct renin inhibitor, or by (pro)renin receptor blocker treatment. The obese phenotype in TGR(hREN) originated from higher food intake, which was partly compensated by increases in resting energy expenditure, total thermogenesis (postprandial and exercise activity), and lipid oxidation during the first 8 weeks of life. Once established, the difference in body weight between TGR(hREN) and SD rats remained constant over time. When restricted to the caloric intake of SD, TGR(hREN) developed an even lower body weight than nontransgenic controls. We did not observe significant changes in the cocaine and amphetamine-regulated transcript, pro-opiomelanocortin, both anorexigenic, or neuropeptide Y, orexigenic, mRNA levels in TGR(hREN) versus SD controls. However, the mRNA level of the agouti-related peptide, orexigenic, was significantly reduced in TGR(hREN) versus SD controls at the end of the study, which indicates a compensatory mechanism. We suggest that the human renin transgene initiates a process leading to increased and early appetite, obesity, and metabolic changes not related to angiotensin II. The mechanisms are independent of any currently known renin-related effects. Key Words: renin-angiotensin system Ⅲ obesity Ⅲ metabolic syndrome Ⅲ ACE inhibitors Ⅲ renin inhibitors Ⅲ (pro)renin receptor Ⅲ handle region peptide O besity is largely responsible for the metabolic syndrome that clusters dyslipidemia, insulin resistance, glucose intolerance/type 2 diabetes mellitus, and hypertension. 1-3 The renin-angiotensin system is fundamental to blood pressure regulation, volume control, and salt balance through the action of angiotensin (Ang) II. 4 Renin is an aspartyl protease that cleaves angiotensinogen, leading to Ang I and subsequently to Ang II formation via the Ang-converting enzyme (ACE). Several renin/prorenin animal models feature metabolic alterations. [5][6][7] Mice solely harboring the human renin gene developed obesity. 7 Rats overexpressing the mouse Ren-2 gene exhibit insulin resistance. 5,6,8 However, this model is not obese, probably because of the severe hypertension and its sequelae. 8 Takahashi et al 9 reported recently that renin-deficient mice (Ren1c Ϫ/Ϫ ) were lean, insulin sensitive, and resistant to diet-induced obesity. Nguyen et al 10 cloned a novel (pro)renin receptor [(P)RR]. The receptor is expressed in a various tissues, including adipocytes. 11 The (P)RR promotes direct renin actions independent of Ang II. 12,13 The binding is specific for renin and prorenin, and the receptor enhances renin catalytic activity and unmasks receptor-bound prorenin catalytic activity. 10 The binding of (pro)renin to the recep...

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“…Using calorimetry, estimates of the energy value of RS are highly variable, ranging from 0 to 11 kJ/g RS in rats and humans (9)(10)(11). Studies in which energetic efficiency of utilization of RS coincide with the in vivo measurement of starch fermentation are scarce (12).…”

Section: Introductionmentioning

confidence: 99%

Quantifying Resistant Starch Using Novel, In Vivo Methodology and the Energetic Utilization of Fermented Starch in Pigs3

Gerrits

Bosch

Borne

2012

The Journal of Nutrition

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To quantify the energy value of fermentable starch, 10 groups of 14 pigs were assigned to one of two dietary treatments comprising diets containing 45% of either pregelatinized (P) or retrograded (R) corn starch. In both diets, a contrast in natural ¹³C enrichment between the starch and nonstarch components of the diet was created to partition between enzymatic digestion and fermentation of the corn starch. Energy and protein retention were measured using indirect calorimetry after adapting the pigs to the diets for 3 wk. Fecal ¹³C enrichment was higher in the R-fed pigs (P < 0.001) and 43% of the R resisted enzymatic digestion. Energy retained as protein was unaffected and energy retained as fat was 29% lower than in P-fed pigs (P < 0.01). Prior to the morning meal, end products of fermentation substantially contributed to substrate oxidation in the R-fed pigs. During the 3-4 h following both meals, heat production was higher (P < 0.05) in P-fed pigs, but this was not preferentially fueled by glucose from corn starch. Digestible energy intake, metabolizable energy intake, and energy retention were reduced (P < 0.05) in R-fed pigs compared with P-fed pigs by 92, 54, and 33 kJ/(kg⁰·⁷⁵ · d), respectively. Therefore, the energy values of fermented resistant starch were 53, 73, and 83% of the digestible, metabolizable, and net energy values of enzymatically degradable starch, respectively. Creating a contrast in natural ¹³C enrichment between starch and nonstarch dietary components provides a promising, noninvasive, in vivo method for estimating the proportion of dietary starch fermented in the gastrointestinal tract.

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Estimation of available energy of dietary fibres by indirect calorimetry in rats

Abstract: Short-term experiments in rats using indirect calorimetry are a suitable method for comparative estimation of the energetic availability of dietary fibres. Results are partly in agreement with values estimated by long-term in vivo methods.

Cited by 21 publications

References 18 publications

New Function for an Old Enzyme: NEP Deficient Mice Develop Late-Onset Obesity

New Function for an Old Enzyme: NEP Deficient Mice Develop Late-Onset Obesity

Energy Metabolism in Human Renin-Gene Transgenic Rats

Quantifying Resistant Starch Using Novel, In Vivo Methodology and the Energetic Utilization of Fermented Starch in Pigs3

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