FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2136799687> ?p ?o ?g. }

• W2136799687 endingPage "R1449" @default.
• W2136799687 startingPage "R1447" @default.
• W2136799687 abstract "CALL FOR PAPERSPhysiological Regulation of AppetiteA peripheral perspective of weight regainPaul S. MacLeanPaul S. MacLeanPublished Online:01 Jun 2005https://doi.org/10.1152/ajpregu.00165.2005MoreSectionsPDF (48 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat body weight regulation is sensitive to a number of environmental, social, and genetic pressures but is ultimately subject to a homeostatic control system linked with adiposity (23, 36). This control system involves a closed-feedback loop between the central nervous system and the peripheral tissues, whereby the central nervous system interprets a complex set of signals from the periphery and subsequently sends signals to defend a certain level of body weight and fat mass. As such, there are metabolic adjustments with overfeeding and weight gain that promote weight loss (22). However, the global obesity epidemic provides evidence that the other pressures affecting body weight cannot only override these protective metabolic adjustments but can also alter the control system in a somewhat permanent fashion by gradually elevating the defended level of adiposity. In addition, there are metabolic adjustments with caloric restriction and weight loss that work to regain the lost weight (22, 24, 26, 27). Although the other pressures affecting body weight can be used to override these metabolic adjustments, there is little evidence of an equivalent readjustment of the control system to lower its targeted adiposity level. It is this persistence of the control system and its metabolic adjustments in the face of downward fluctuations in adiposity that explain the most critical problem in obesity treatment: keeping the weight off after weight loss. It is for this reason that significant efforts have been made to increase our understanding of the metabolic drive to regain weight.One of the most fundamental metabolic adjustments in response to weight reduction is the large positive energy imbalance, or “energy gap,” between intake and expenditure (26). In both humans and rodents, the drive to consume food increases and energy expenditure decreases. In order to maintain the reduced weight, the food provision must be reduced to match the suppressed level of expenditure. When this limitation on food provision is not maintained, food is ingested in gross excess of expenditure, the extra energy is stored, and weight is gained. In this issue of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Evans et al. (9) report an interesting set of observations that describe this metabolic drive in two strains of rats in response to two weeks of caloric restriction. These authors have used an impressive array of metabolic monitoring tools to follow these animals prospectively through caloric restriction and the early part of the relapse to the defended body weight. Long-Evans rats responded with hyperphagia that was persistently higher than ad libitum-fed controls through 8 days of refeeding, while expenditure appeared to resolve within a few days. In contrast, the Sprague-Dawley rats had an expenditure that was still suppressed after 8 days of refeeding, while intake was higher for only the first day. The authors use this divergent response to suggest that the homeostatic response to caloric restriction may selectively target appetite or expenditure to restore body weight.As Evans et al. (9) have pointed out in their discussion, there are neural pathways that have a more profound influence on one side of the energy balance equation, and there may be others yet unidentified that are even more specific for intake or expenditure. Complicating the distinction is the thermic effect of food, which effectively increases expenditure as more food is consumed. In any case, the practical lesson from this interesting study is that differential genetic pressures may yield divergent responses to energy restriction in order to achieve the same energy gap and rate of weight regain. This is a critical consideration when pursuing therapeutic strategies that target the metabolic drive to regain for the purposes of facilitating sustained weight reduction. The implication is that therapies targeting a single factor or component of the metabolic drive to regain weight may not be effective for everyone. It is not surprising that exercise, with broad and numerous effects on metabolism, appears to be the most potent approach to facilitating sustained weight reduction (3, 18, 19, 23).While much attention has been given to the neural pathways that are involved in the regulation of energy balance, less has been given to other metabolic adjustments in the periphery that contribute to the drive to regain. Indirect evidence of one such adjustment comes from the respiratory quotient (RQ) observed by Evans et al. (9) and others (6, 12, 27). During regain when there is a chronic positive energy balance, there is also a dramatic shift in fuel utilization that promotes an energetically efficient deposition of fat stores (8). Glucose becomes the preferred fuel for energy needs, and fatty acid oxidation is suppressed. The consequence is the diversion of ingested fats to the adipose stores (4). This shift is important in that the ingested lipid is stored with little energetic expense, while glucose must go through the energetic costly process of lipogenesis (10). Therefore, for the same amount of consumed energy, more weight will be gained if the ingested fat is stored and the carbohydrate is used for energy. One additional consideration in this discussion, however, is that de novo lipogenesis is likely occurring during weight regain, an effect that will elevate RQ and make it less reflective of substrate oxidation (13). As Evans et al. (9) point out in their study, the RQ above 1.0 in refeeding rats is a fairly good indication that a significant amount of lipogenesis is occurring (1). Without fuel tracers, it is difficult to distinguish between the respective contribution of the shift in fuel oxidation and of lipogenesis to the elevation in RQ. However, under these conditions of a large positive energy gap, it is likely that both are occurring. The result is the preferential use of carbohydrates for energy, the diversion of ingested lipid into fat stores, and the conversion of any excess glucose to fat. This effectively increases the rate of weight regain during the refeeding period.The underlying mechanisms that are responsible for these dramatic changes in fuel metabolism can be linked to the large energy imbalance and the accompanying excursions in circulating levels of glucose and insulin throughout the day. First, insulin has potent suppressive effects on the release of endogenously stored lipid (16). Depending on the size of the lipid component in the diet, this antilipolytic effect would likely lead to reduced fatty acid availability in hepatic and skeletal muscle. Second, insulin and glucose lead to the production of malonyl-CoA (6, 32, 35). Malonyl-CoA is not only a potent inhibitor of carnitine palmitoyl transferase I (2, 28), but it also is the required substrate for fatty acid synthetase. As such, the elevation of malonyl-CoA suppresses fatty acid oxidation while directing excess substrate to de novo lipogenesis. When energy restriction is followed by ad libitum feeding, studies have consistently shown an elevation in malonyl-CoA and a suppression in fat oxidation (30–32).In addition to these immediate effects on lipolysis and tissue metabolism, insulin and glucose induce the expression of a host of genes in the liver, muscle, and adipose tissue that have a more sustained effect on fuel metabolism. There is substantial evidence that these effects are mediated, at least in part, by sterol response element binding protein 1c (SREBP-1c) (11, 15, 20, 21, 34). A number of models that have employed a period of energy restriction followed by refeeding have shown that SREBP-1c and its target genes are dramatically induced in liver, adipose, and skeletal muscle tissues (5, 7, 14, 17, 29, 33). The direct and indirect targets of SREBP-1c are enzymes that promote oxidation of carbohydrates and the synthesis and accumulation of fatty acids and triglycerides. SREBP-1c has been implicated in increasing the expression of acetyl-CoA carboxylase, fatty acid synthase, ATP-citrate lyase, and a number of genes in the glycolytic pathway. The consequences of increased SREBP-1c expression are an enzymatic profile with enhanced glycolytic and lipogenic capacities, essentially magnifying the immediate effects of insulin and glucose on fuel metabolism in these tissues.There are two reasons why these peripheral aspects of fuel metabolism may be important to consider in the process of weight regain. First, because it is energetically efficient, the trafficking of ingested fats into the adipose depots contributes to a higher rate of regain and a quicker return to the defended level of adiposity. Second, an increased capacity to clear excess fuels into the lipid depots may act through nutrient sensing systems (25) to extend or increase bouts of feeding, a continuing positive energy balance, and further weight gain. Within this scheme, the rate of regain declines as the capacity of adipose tissue limits the ability of these peripheral metabolic adjustments to traffic ingested fats to adipose tissues and rapidly clear excess fuels. Although these metabolic adjustments in the periphery would not be expected to explain all aspects of weight regain, they may be playing a significant role in the high rates of relapse to the obese state in humans. Undoubtedly, the substantial progress in recent years that has furthered our understanding of the neural pathways that are involved in body weight regulation (23, 36) will be critical in designing effective strategies that counter the metabolic drive to regain weight after weight loss. It is critical to remember, however, that the signals controlling those pathways are likely to come from the periphery, where the weight actually lies. From a peripheral perspective, it is this researcher’s opinion that we need to further our understanding of fuel utilization and accumulation during the process of regaining lost weight, and how the flux through these pathways link to the neural pathways controlling energy balance.GRANTSP. S. MacLean is supported by grants from the U.S. Department of Health and Human Services and National Institute of Diabetes and Digestive and Kidney Diseases Grants DK-038088 and DK-067403.REFERENCES1 Acheson KJ, Schutz Y, Bessard T, Flatt JP, and Jequier E. Carbohydrate metabolism and de novo lipogenesis in human obesity. Am J Clin Nutr 45: 78–85, 1987.Crossref | PubMed | ISI | Google Scholar2 Alam N and Saggerson ED. Malonyl-CoA and the regulation of fatty acid oxidation in soleus muscle. Biochem J 334: 233–241, 1998.Crossref | PubMed | ISI | Google Scholar3 Anderson JW, Konz EC, Frederich RC, and Wood CL. Long-term weight-loss maintenance: a meta-analysis of US studies. Am J Clin Nutr 74: 579–584, 2001.Crossref | PubMed | ISI | Google Scholar4 Bessesen DH, Rupp CL, and Eckel RH. Dietary fat is shunted away from oxidation, toward storage in obese Zucker rats. Obes Res 3: 179–189, 1995.Crossref | PubMed | Google Scholar5 Bizeau ME, MacLean PS, Johnson GC, and Wei Y. Skeletal muscle sterol regulatory element binding protein-1c decreases with food deprivation and increases with feeding in rats. J Nutr 133: 1787–1792, 2003.Crossref | PubMed | ISI | Google Scholar6 Chien D, Dean D, Saha AK, Flatt JP, and Ruderman NB. Malonyl-CoA content and fatty acid oxidation in rat muscle and liver in vivo. Am J Physiol Endocrinol Metab 279: E259–E265, 2000.Link | ISI | Google Scholar7 Commerford SR, Peng L, Dube JJ, and O’Doherty RM. In vivo regulation of SREBP-1c in skeletal muscle: effects of nutritional status, glucose, insulin, and leptin. Am J Physiol Regul Integr Comp Physiol 287: R218–R227, 2004.Link | ISI | Google Scholar8 Dulloo AG and Jacquet J. An adipose-specific control of thermogenesis in body weight regulation. Int J Obes Relat Metab Disord 25, Suppl 5: S22–S29, 2001.Google Scholar9 Evans SA, Messina MM, Knight WD, Parsons AD, and Overton JM. Long-Evans and Sprague-Dawley rats exhibit divergent responses to refeeding after caloric restriction. Am J Physiol Regul Integr Comp Physiol 288: R1468–R1476, 2005.Link | ISI | Google Scholar10 Flatt JP and Tremblay A. Energy expenditure and substrate oxidation. In: Handbook of Obesity, edited by Bray GA, Bouchard C and James WPT. New York: Decker, 1998, p. 513–537.Google Scholar11 Foretz M, Pacot C, Dugail I, Lemarchand P, Guichard C, Le Liepvre X, Berthelier-Lubrano C, Spiegelman B, Kim JB, Ferre P, and Foufelle F. ADD1/SREBP-1c is required in the activation of hepatic lipogenic gene expression by glucose. Mol Cell Biol 19: 3760–3768, 1999.Crossref | PubMed | ISI | Google Scholar12 Froidevaux F, Schutz Y, Christin L, and Jequier E. Energy expenditure in obese women before and during weight loss, after refeeding, and in the weight-relapse period. Am J Clin Nutr 57: 35–42, 1993.Crossref | PubMed | ISI | Google Scholar13 Glamour TS, McCullough AJ, Sauer PJ, and Kalhan SC. Quantification of carbohydrate oxidation by respiratory gas exchange and isotopic tracers. Am J Physiol Endocrinol Metab 268: E789–E796, 1995.Link | ISI | Google Scholar14 Gosmain Y, Dif N, Berbe V, Loizon E, Rieusset J, Vidal H, and Lefai E. Regulation of SREBP-1 expression and transcriptional action on HKII and FAS genes during fasting and refeeding in rat tissues. J Lipid Res 2005.Google Scholar15 Guillet-Deniau I, Pichard AL, Kone A, Esnous C, Nieruchalski M, Girard J, and Prip-Buus C. Glucose induces de novo lipogenesis in rat muscle satellite cells through a sterol-regulatory-element-binding-protein-1c-dependent pathway. J Cell Sci 117: 1937–1944, 2004.Crossref | PubMed | ISI | Google Scholar16 Hales CN, Luzio JP, and Siddle K. Hormonal control of adipose-tissue lipolysis. Biochem Soc Symp: 97–135, 1978.PubMed | Google Scholar17 Horton JD, Bashmakov Y, Shimomura I, and Shimano H. Regulation of sterol regulatory element binding proteins in livers of fasted and refed mice. Proc Natl Acad Sci USA 95: 5987–5992, 1998.Crossref | PubMed | ISI | Google Scholar18 Jakicic JM, Winters C, Lang W, and Wing RR. Effects of intermittent exercise and use of home exercise equipment on adherence, weight loss, and fitness in overweight women: a randomized trial. JAMA 282: 1554–1560, 1999.Crossref | PubMed | ISI | Google Scholar19 Klem ML, Wing RR, McGuire MT, Seagle HM, and Hill JO. A descriptive study of individuals successful at long-term maintenance of substantial weight loss. Am J Clin Nutr 66: 239–246, 1997.Crossref | PubMed | ISI | Google Scholar20 Kotzka J, Muller-Wieland D, Koponen A, Njamen D, Kremer L, Roth G, Munck M, Knebel B, and Krone W. ADD1/SREBP-1c mediates insulin-induced gene expression linked to the MAP kinase pathway. Biochem Biophys Res Commun 249: 375–379, 1998.Crossref | PubMed | ISI | Google Scholar21 Kotzka J, Muller-Wieland D, Roth G, Kremer L, Munck M, Schurmann S, Knebel B, and Krone W. Sterol regulatory element binding proteins (SREBP)-1a and SREBP-2 are linked to the MAP-kinase cascade. J Lipid Res 41: 99–108, 2000.Crossref | PubMed | ISI | Google Scholar22 Leibel RL, Rosenbaum M, and Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med 332: 621–628, 1995.Crossref | PubMed | ISI | Google Scholar23 Levin BE. The drive to regain is mainly in the brain. Am J Physiol Regul Integr Comp Physiol 287: R1297–R1300, 2004.Link | ISI | Google Scholar24 Levin BE and Dunn-Meynell AA. Chronic exercise lowers the defended body weight gain and adiposity in diet-induced obese rats. Am J Physiol Regul Integr Comp Physiol 286: R771–R778, 2004.Link | ISI | Google Scholar25 Levin BE, Routh VH, Kang L, Sanders NM, and Dunn-Meynell AA. Neuronal glucosensing: what do we know after 50 years? Diabetes 53: 2521–2528, 2004.Crossref | PubMed | ISI | Google Scholar26 MacLean PS, Higgins JA, Johnson GC, Fleming-Elder BK, Donahoo WT, Melanson EL, and Hill JO. Enhanced metabolic efficiency contributes to weight regain after weight loss in obesity-prone rats. Am J Physiol Regul Integr Comp Physiol 287: R1306–R1315, 2004.Link | ISI | Google Scholar27 MacLean PS, Higgins JA, Johnson GC, Fleming-Elder BK, Peters JC, and Hill JO. Metabolic adjustments with the development, treatment, and recurrence of obesity in obesity-prone rats. Am J Physiol Regul Integr Comp Physiol 287: R288–R297, 2004.Link | ISI | Google Scholar28 McGarry JD, Sen A, Esser V, Woeltje KF, Weis B, and Foster DW. New insights into the mitochondrial carnitine palmitoyltransferase enzyme system. Biochimie 73: 77–84, 1991.Crossref | PubMed | ISI | Google Scholar29 Minehira K, Vega N, Vidal H, Acheson K, and Tappy L. Effect of carbohydrate overfeeding on whole body macronutrient metabolism and expression of lipogenic enzymes in adipose tissue of lean and overweight humans. Int J Obes Relat Metab Disord 28: 1291–1298, 2004.Crossref | PubMed | ISI | Google Scholar30 Moir AM and Zammit VA. Monitoring of changes in hepatic fatty acid and glycerolipid metabolism during the starved-to-fed transition in vivo. Studies on awake, unrestrained rats. Biochem J 289: 49–55, 1993.Crossref | PubMed | ISI | Google Scholar31 Moir AM and Zammit VA. Rapid switch of hepatic fatty acid metabolism from oxidation to esterification during diurnal feeding of meal-fed rats correlates with changes in the properties of acetyl-CoA carboxylase, but not of carnitine palmitoyltransferase I. Biochem J 291: 241–246, 1993.Crossref | PubMed | ISI | Google Scholar32 Saha AK, Laybutt DR, Dean D, Vavvas D, Sebokova E, Ellis B, Klimes I, Kraegen EW, Shafrir E, and Ruderman NB. Cytosolic citrate and malonyl-CoA regulation in rat muscle in vivo. Am J Physiol Endocrinol Metab 276: E1030–E1037, 1999.Link | ISI | Google Scholar33 Shimano H, Yahagi N, Amemiya-Kudo M, Hasty AH, Osuga J, Tamura Y, Shionoiri F, Iizuka Y, Ohashi K, Harada K, Gotoda T, Ishibashi S, and Yamada N. Sterol regulatory element-binding protein-1 as a key transcription factor for nutritional induction of lipogenic enzyme genes. J Biol Chem 274: 35832–35839, 1999.Crossref | PubMed | ISI | Google Scholar34 Shimomura I, Bashmakov Y, Ikemoto S, Horton JD, Brown MS, and Goldstein JL. Insulin selectively increases SREBP-1c mRNA in the livers of rats with streptozotocin-induced diabetes. Proc Natl Acad Sci USA 96: 13656–13661, 1999.Crossref | PubMed | ISI | Google Scholar35 Winder WW and Holmes BF. Insulin stimulation of glucose uptake fails to decrease palmitate oxidation in muscle if AMPK is activated. J Appl Physiol 89: 2430–2437, 2000.Link | ISI | Google Scholar36 Woods SC, Benoit SC, Clegg DJ, and Seeley RJ. Clinical endocrinology and metabolism. Regulation of energy homeostasis by peripheral signals. Best Pract Res Clin Endocrinol Metab 18: 497–515, 2004.Crossref | PubMed | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: P. S. MacLean, UCDHSC @ Fitzsimons, Center for Human Nutrition, PO Box 6511, F-8305, Aurora, CO 80045 (E-mail: [email protected]) Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationCited By2014 AAHA Weight Management Guidelines for Dogs and Cats* †Journal of the American Animal Hospital Association, Vol. 50, No. 1Repletion of TNFα or leptin in calorically restricted mice suppresses post-restriction hyperphagiaDisease Models & Mechanisms, Vol. 5, No. 1Low-carbohydrate High-fat Diets: Regulation of Energy Balance and Body Weight Regain in Rats6 September 2012 | Obesity, Vol. 17, No. 2Peripheral metabolic responses to prolonged weight reduction that promote rapid, efficient regain in obesity-prone ratsPaul S. MacLean, Janine A. Higgins, Matthew R. Jackman, Ginger C. Johnson, Brooke K. Fleming-Elder, Holly R. Wyatt, Edward L. Melanson, and James O. Hill1 June 2006 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 290, No. 6Compensatory response to reducing body weightDrug Discovery Today: Disease Mechanisms, Vol. 2, No. 3 More from this issue > Volume 288Issue 6June 2005Pages R1447-R1449 Copyright & PermissionsCopyright © 2005 the American Physiological Societyhttps://doi.org/10.1152/ajpregu.00165.2005PubMed15886355History Published online 1 June 2005 Published in print 1 June 2005 Metrics" @default.
• W2136799687 created "2016-06-24" @default.
• W2136799687 creator A5043317034 @default.
• W2136799687 date "2005-06-01" @default.
• W2136799687 modified "2023-09-25" @default.
• W2136799687 title "A peripheral perspective of weight regain" @default.
• W2136799687 cites W131343593 @default.
• W2136799687 cites W1784510045 @default.
• W2136799687 cites W1899239231 @default.
• W2136799687 cites W1902023877 @default.
• W2136799687 cites W1993959691 @default.
• W2136799687 cites W1995588427 @default.
• W2136799687 cites W2003527036 @default.
• W2136799687 cites W2024900170 @default.
• W2136799687 cites W2027080215 @default.
• W2136799687 cites W2027976419 @default.
• W2136799687 cites W2030610610 @default.
• W2136799687 cites W2034046497 @default.
• W2136799687 cites W2038890731 @default.
• W2136799687 cites W2046220668 @default.
• W2136799687 cites W2055610261 @default.
• W2136799687 cites W2065296010 @default.
• W2136799687 cites W2080010303 @default.
• W2136799687 cites W2097309757 @default.
• W2136799687 cites W2103119919 @default.
• W2136799687 cites W2114960748 @default.
• W2136799687 cites W2115727039 @default.
• W2136799687 cites W2120025309 @default.
• W2136799687 cites W2120292775 @default.
• W2136799687 cites W2129747400 @default.
• W2136799687 cites W2138680533 @default.
• W2136799687 cites W2142247098 @default.
• W2136799687 cites W2148323125 @default.
• W2136799687 cites W2157416148 @default.
• W2136799687 cites W2158465207 @default.
• W2136799687 cites W2165570733 @default.
• W2136799687 cites W2278428315 @default.
• W2136799687 cites W2316534927 @default.
• W2136799687 cites W2395276330 @default.
• W2136799687 cites W4238765814 @default.
• W2136799687 doi "https://doi.org/10.1152/ajpregu.00165.2005" @default.
• W2136799687 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15886355" @default.
• W2136799687 hasPublicationYear "2005" @default.
• W2136799687 type Work @default.
• W2136799687 sameAs 2136799687 @default.
• W2136799687 citedByCount "7" @default.
• W2136799687 countsByYear W21367996872012 @default.
• W2136799687 countsByYear W21367996872013 @default.
• W2136799687 countsByYear W21367996872014 @default.
• W2136799687 crossrefType "journal-article" @default.
• W2136799687 hasAuthorship W2136799687A5043317034 @default.
• W2136799687 hasConcept C126322002 @default.
• W2136799687 hasConcept C12713177 @default.
• W2136799687 hasConcept C154945302 @default.
• W2136799687 hasConcept C15744967 @default.
• W2136799687 hasConcept C41008148 @default.
• W2136799687 hasConcept C46762472 @default.
• W2136799687 hasConcept C71924100 @default.
• W2136799687 hasConceptScore W2136799687C126322002 @default.
• W2136799687 hasConceptScore W2136799687C12713177 @default.
• W2136799687 hasConceptScore W2136799687C154945302 @default.
• W2136799687 hasConceptScore W2136799687C15744967 @default.
• W2136799687 hasConceptScore W2136799687C41008148 @default.
• W2136799687 hasConceptScore W2136799687C46762472 @default.
• W2136799687 hasConceptScore W2136799687C71924100 @default.
• W2136799687 hasIssue "6" @default.
• W2136799687 hasLocation W21367996871 @default.
• W2136799687 hasOpenAccess W2136799687 @default.
• W2136799687 hasPrimaryLocation W21367996871 @default.
• W2136799687 hasRelatedWork W1670566515 @default.
• W2136799687 hasRelatedWork W1975467175 @default.
• W2136799687 hasRelatedWork W2095322754 @default.
• W2136799687 hasRelatedWork W2098170879 @default.
• W2136799687 hasRelatedWork W2149537132 @default.
• W2136799687 hasRelatedWork W2605852498 @default.
• W2136799687 hasRelatedWork W2748952813 @default.
• W2136799687 hasRelatedWork W2899084033 @default.
• W2136799687 hasRelatedWork W4250032403 @default.
• W2136799687 hasRelatedWork W641279757 @default.
• W2136799687 hasVolume "288" @default.
• W2136799687 isParatext "false" @default.
• W2136799687 isRetracted "false" @default.
• W2136799687 magId "2136799687" @default.
• W2136799687 workType "article" @default.