Relevant bibliographies by topics / Thrifty genotype / Journal articles

Journal articles on the topic 'Thrifty genotype'

To see the other types of publications on this topic, follow the link: Thrifty genotype.
Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Thrifty genotype.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Allen, John S., and Susan M. Cheer. "The Non-Thrifty Genotype." Current Anthropology 37, no. 5 (December 1996): 831–42. http://dx.doi.org/10.1086/204566.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Colagiuri, S., J. S. Allen, J. C. Brand Miller, and S. M. Cheer. "The thrifty genotype hypothesis." Diabetic Medicine 14, no. 6 (June 1997): 504. http://dx.doi.org/10.1002/(sici)1096-9136(199706)14:6<504::aid-dia392>3.0.co;2-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Neel, James V. "The “Thrifty Genotype” in 19981." Nutrition Reviews 57, no. 5 (April 27, 2009): 2–9. http://dx.doi.org/10.1111/j.1753-4887.1999.tb01782.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Zafon, C. "Ageing purpose: another thrifty genotype." Medical Hypotheses 61, no. 4 (October 2003): 482–85. http://dx.doi.org/10.1016/s0306-9877(03)00201-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Stern, Michael P., Mary Bartley, Ravindranath Duggirala, and Benjamin Bradshaw. "Birth weight and the Metabolic Syndrome: thrifty phenotype or thrifty genotype?" Diabetes/Metabolism Research and Reviews 16, no. 2 (March 2000): 88–93. http://dx.doi.org/10.1002/(sici)1520-7560(200003/04)16:2<88::aid-dmrr81>3.0.co;2-m.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Bindon, James R., and Paul T. Baker. "Bergmann's rule and the thrifty genotype." American Journal of Physical Anthropology 104, no. 2 (October 1997): 201–10. http://dx.doi.org/10.1002/(sici)1096-8644(199710)104:2<201::aid-ajpa6>3.0.co;2-0.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

McCance, D. R., D. J. Pettitt, R. L. Hanson, L. T. H. Jacobsson, W. C. Knowler, and P. H. Bennett. "Birth weight and non-insulin dependent diabetes: thrifty genotype, thrifty phenotype, or surviving small baby genotype?" BMJ 308, no. 6934 (April 9, 1994): 942–45. http://dx.doi.org/10.1136/bmj.308.6934.942.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Prentice, Andrew M., Pura Rayco-Solon, and Sophie E. Moore. "Insights from the developing world: thrifty genotypes and thrifty phenotypes." Proceedings of the Nutrition Society 64, no. 2 (May 2005): 153–61. http://dx.doi.org/10.1079/pns2005421.

Full text
Abstract:
Few researchers would dispute that the pandemic of obesity is caused by a profound mismatch between humanity's present environmental circumstances and those that have moulded evolutionary selection. This concept was first articulated when gestational diabetes was described as being the result of a ‘thrifty genotype rendered detrimental by progress’. More recently, this hypothesis has been extended to the concept of a ‘thrifty phenotype’ to describe the metabolic adaptations adopted as a survival strategy by a malnourished fetus; changes that may also be inappropriate to deal with a later life of affluence. Both the thrifty genotype and the thrifty phenotype hypotheses would predict that populations in some areas of the developing world would be at greater risk of obesity and its co-morbidities; a proposition to be explored in the present paper. To date thrifty genes remain little more than a nebulous concept propagated by the intuitive logic that man has been selected to survive episodic famine and seasonal hungry periods. Under such conditions those individuals who could lay down extra energy stores and use them most efficiently would have a survival advantage. The search for candidate thrifty genes needs to cover every aspect of human energy balance from food-seeking behaviour to the coupling efficiency of oxidative phosphorylation. The present paper will describe examples of attempts to find thrifty genes in three selected candidate areas: maternally-transmitted mitochondrial genes; the uncoupling proteins; apoE4, whose geographical distribution has been linked to a possible thrifty role in lipoprotein and cholesterol metabolism.
APA, Harvard, Vancouver, ISO, and other styles
9

Wendorf, M., and I. D. Goldfine. "Archaeology of NIDDM: Excavation of the "Thrifty" Genotype." Diabetes 40, no. 2 (February 1, 1991): 161–65. http://dx.doi.org/10.2337/diab.40.2.161.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Dowse, G., and P. Zimmet. "The thrifty genotype in non-insulin dependent diabetes." BMJ 306, no. 6877 (February 27, 1993): 532–33. http://dx.doi.org/10.1136/bmj.306.6877.532.

Full text
APA, Harvard, Vancouver, ISO, and other styles
11

Fox, R. "The thrifty genotype and non-insulin dependent diabetes." BMJ 306, no. 6882 (April 3, 1993): 933. http://dx.doi.org/10.1136/bmj.306.6882.933-b.

Full text
APA, Harvard, Vancouver, ISO, and other styles
12

Garrow, J. "The thrifty genotype and non-insulin dependent diabetes." BMJ 306, no. 6882 (April 3, 1993): 933–34. http://dx.doi.org/10.1136/bmj.306.6882.933-c.

Full text
APA, Harvard, Vancouver, ISO, and other styles
13

Cruickshank, K. "The thrifty genotype and non-insulin dependent diabetes." BMJ 306, no. 6882 (April 3, 1993): 934. http://dx.doi.org/10.1136/bmj.306.6882.934.

Full text
APA, Harvard, Vancouver, ISO, and other styles
14

Bradley, P. J. "The thrifty genotype in non-insulin dependent diabetes." BMJ 306, no. 6886 (May 1, 1993): 1198. http://dx.doi.org/10.1136/bmj.306.6886.1198-b.

Full text
APA, Harvard, Vancouver, ISO, and other styles
15

Wendorf, M., and I. D. Goldfine. "Archaeology of NIDDM. Excavation of the "thrifty" genotype." Diabetes 40, no. 2 (February 1, 1991): 161–65. http://dx.doi.org/10.2337/diabetes.40.2.161.

Full text
APA, Harvard, Vancouver, ISO, and other styles
16

Rubio-Ruiz, María Esther, Ana Elena Peredo-Escárcega, Agustina Cano-Martínez, and Verónica Guarner-Lans. "An Evolutionary Perspective of Nutrition and Inflammation as Mechanisms of Cardiovascular Disease." International Journal of Evolutionary Biology 2015 (November 29, 2015): 1–10. http://dx.doi.org/10.1155/2015/179791.

Full text
Abstract:
When cardiovascular diseases are viewed from an evolutionary biology perspective, a heightened thrifty and an inflammatory design could be their mechanisms. Human ancestors confronted a greater infectious load and were subjected to the selection for proinflammatory genes and a strong inflammatory function. Ancestors also faced starvation periods that pressed for a thrifty genotype which caused fat accumulation. The pressure of sustaining gluconeogenesis during periods of poor nourishment selected individuals with insulin resistance. Obesity induces a proinflammatory state due to the secretion of adipokines which underlie cardiometabolic diseases. Our actual lifestyle needs no more of such proinflammatory and thrifty genotypes and these ancestral genes might increase predisposition to diseases. Risk factors for atherosclerosis and diabetes are based on inflammatory and genetic foundations that can be accounted for by excess fat. Longevity has also increased in recent times and is related to a proinflammatory response with cardiovascular consequences. If human ancestral lifestyle could be recovered by increasing exercise and adapting a calorie restriction diet, obesity would decrease and the effects on chronic low-grade inflammation would be limited. Thereby, the rates of both atherosclerosis and diabetes could be reduced.
APA, Harvard, Vancouver, ISO, and other styles
17

Fee, Margery. "Racializing narratives: Obesity, diabetes and the “Aboriginal” thrifty genotype." Social Science & Medicine 62, no. 12 (June 2006): 2988–97. http://dx.doi.org/10.1016/j.socscimed.2005.11.062.

Full text
APA, Harvard, Vancouver, ISO, and other styles
18

Osada, Hisao. "Association between Polymorphisms in Genes Related to Common Adult Diseases and Fetal Growth." Clinical medicine. Pediatrics 3 (January 2009): CMPed.S2154. http://dx.doi.org/10.4137/cmped.s2154.

Full text
Abstract:
A close relationship between size at birth and occurrence of common adult diseases has been reported. As an explanation of this relationship, it has been hypothesized that the thrifty genotypes cause changes in growth efficiency during fetal period and diseases in later life. In the present study, we examined the association of fetal growth with genetic polymorphisms within the IGF2-INS-TH region and in the G protein gene. Analysis of the genes in the IGF2-INS-TH region suggests that thrifty genotype has the effect of accelerating fetal growth, but at the same time a genomic imprinting mechanism is also involved. Analysis of the G protein β3 subunit gene unveiled that the 825T allele in the mother may exert influence on fetal metabolic environment. By extending the analysis to other genomic regions related to common adult diseases using the same technique, the detailed role of genetic polymorphisms may be elucidated.
APA, Harvard, Vancouver, ISO, and other styles
19

Bouchard, C. "The biological predisposition to obesity: beyond the thrifty genotype scenario." International Journal of Obesity 31, no. 9 (March 13, 2007): 1337–39. http://dx.doi.org/10.1038/sj.ijo.0803610.

Full text
APA, Harvard, Vancouver, ISO, and other styles
20

Reaven, G. M. "Hypothesis: muscle insulin resistance is the ("not-so") thrifty genotype." Diabetologia 41, no. 4 (March 20, 1998): 482–84. http://dx.doi.org/10.1007/s001250050933.

Full text
APA, Harvard, Vancouver, ISO, and other styles
21

Propping, P., Charlotte Hohenschutz, and V. Voigtl�nder. "Increased birth weight in psoriasis ?Another expression of a ?thrifty genotype??" Human Genetics 71, no. 1 (September 1985): 92. http://dx.doi.org/10.1007/bf00295677.

Full text
APA, Harvard, Vancouver, ISO, and other styles
22

Cone, Roger D. "Haploinsufficiency of the melanocortin-4 receptor: part of a thrifty genotype?" Journal of Clinical Investigation 106, no. 2 (July 15, 2000): 185–87. http://dx.doi.org/10.1172/jci10628.

Full text
APA, Harvard, Vancouver, ISO, and other styles
23

Swinburn, B. A. "The Thrifty Genotype Hypothesis: How Does it Look After 30 Years?" Diabetic Medicine 13, no. 8 (August 1996): 695–99. http://dx.doi.org/10.1002/(sici)1096-9136(199608)13:8<695::aid-dia170>3.0.co;2-#.

Full text
APA, Harvard, Vancouver, ISO, and other styles
24

Berbesque, J. Colette, Frank W. Marlowe, Peter Shaw, and Peter Thompson. "Hunter–gatherers have less famine than agriculturalists." Biology Letters 10, no. 1 (January 2014): 20130853. http://dx.doi.org/10.1098/rsbl.2013.0853.

Full text
Abstract:
The idea that hunter–gatherer societies experience more frequent famine than societies with other modes of subsistence is pervasive in the literature on human evolution. This idea underpins, for example, the ‘thrifty genotype hypothesis’. This hypothesis proposes that our hunter–gatherer ancestors were adapted to frequent famines, and that these once adaptive ‘thrifty genotypes’ are now responsible for the current obesity epidemic. The suggestion that hunter–gatherers are more prone to famine also underlies the widespread assumption that these societies live in marginal habitats. Despite the ubiquity of references to ‘feast and famine’ in the literature describing our hunter–gatherer ancestors, it has rarely been tested whether hunter–gatherers suffer from more famine than other societies. Here, we analyse famine frequency and severity in a large cross-cultural database, in order to explore relationships between subsistence and famine risk. This is the first study to report that, if we control for habitat quality, hunter–gatherers actually had significantly less—not more—famine than other subsistence modes. This finding challenges some of the assumptions underlying for models of the evolution of the human diet, as well as our understanding of the recent epidemic of obesity and type 2 diabetes mellitus.
APA, Harvard, Vancouver, ISO, and other styles
25

Aisyah, Riandini, Ahmad Hamim Sadewa, Suryono Yudha Patria, and Abdul Wahab. "The PPARGC1A Is the Gene Responsible for Thrifty Metabolism Related Metabolic Diseases: A Scoping Review." Genes 13, no. 10 (October 18, 2022): 1894. http://dx.doi.org/10.3390/genes13101894.

Full text
Abstract:
The “thrifty genotype” hypothesis has thus far described the relationship between specific genes and the population’s resilience to food scarcity circumstances, but its link to the widespread prevalence of genetic diseases and metabolic syndrome has not been adequately mapped. The purpose of the study was to discover genes responsible for thrifty metabolism. A systematic search with keywords was performed for relevant titles. This study used the article’s database published by Pubmed, Proquest, and EBSCO from 2009 to 2019. Out of 380 papers screened for eligibility, the final evaluation determined that five studies should be included in the analysis. Results indicated that PPARGC1A Gly482Ser led to high BMI in the Tongans population but was unrelated to the onset of type 2 diabetes mellitus, but this was not the case in the Maori population. Significantly differing frequencies of PPAR C1431T and Pro12Ala gene polymorphisms were observed in the Iranian population. GWAS identification of additional genes in Asian and European populations did not produce consistent findings. As a summary, PPARGC1A Gly482Ser addresses as the gene responsible for thrifty metabolism in the Pacific population although some studies show inconsistent results.
APA, Harvard, Vancouver, ISO, and other styles
26

Rawson, HM, and JM Clarke. "Nocturnal Transpiration in Wheat." Functional Plant Biology 15, no. 3 (1988): 397. http://dx.doi.org/10.1071/pp9880397.

Full text
Abstract:
Over the night, stomata of wheat leaves took several hours to reach their most closed position and began to open some hours before dawn. The pattern and amount of night transpiration was changed by current vapour pressure deficit (VPD) but not by VPD or transpiration during the previous day. Mean night transpiration per unit VPD was unchanged by current VPD. Night transpiration of whole plants increased linearly with VPD though genotypes differed significantly in amount. The most profligate genotype transpired at 50 g m-2 leaf h-1 at a VPD of 30 mbar which was twice the rate of the most thrifty genotype. Attempts were made to estimate the proportion of night transpiration occurring through the stomata and the cuticle by three methods: comparisons of stressed and unstressed leaves, wilting patterns of detached leaves, and transpiration rates of detached leaves in ABA solutions. The methods gave equivalent rankings of the genotypes and similar absolute values for the 'cuticular component', which contributed 13-50% of total night transpiration. We conclude that transpiration could exceed 0.5 mm per night in unstressed crops, though this would be considerably reduced by selection of genotypes with both low cuticular and low stomatal transpiration.
APA, Harvard, Vancouver, ISO, and other styles
27

Naber, C., R. Erbel, and W. Siffert. "The G Protein β3 Subunit Gene (GNB3) 825T Allele - a Thrifty Genotype." Current Genomics 4, no. 4 (May 1, 2003): 337–42. http://dx.doi.org/10.2174/1389202033490358.

Full text
APA, Harvard, Vancouver, ISO, and other styles
28

Reddon, H., Y. Patel, M. Turcotte, M. Pigeyre, and D. Meyre. "Revisiting the evolutionary origins of obesity: lazy versus peppy-thrifty genotype hypothesis." Obesity Reviews 19, no. 11 (September 27, 2018): 1525–43. http://dx.doi.org/10.1111/obr.12742.

Full text
APA, Harvard, Vancouver, ISO, and other styles
29

Paradies, Yin, M. J. Montoya, and Stephanie M. Fullerton. "Racialized Genetics and the Study of Complex Diseases: The Thrifty Genotype Revisited." Perspectives in Biology and Medicine 50, no. 2 (2007): 203–27. http://dx.doi.org/10.1353/pbm.2007.0020.

Full text
APA, Harvard, Vancouver, ISO, and other styles
30

Astiz, S., A. Gonzalez-Bulnes, I. Astiz, A. Barbero, M. L. Perez-Solana, and I. Garcia-Real. "Advanced onset of puberty after metformin therapy in swine with thrifty genotype." Experimental Physiology 99, no. 9 (September 1, 2014): 1241–52. http://dx.doi.org/10.1113/expphysiol.2014.081455.

Full text
APA, Harvard, Vancouver, ISO, and other styles
31

Poulton, Joanna. "Does a common mitochondrial DNA polymorphism underlie susceptibility to diabetes and the thrifty genotype?" Trends in Genetics 14, no. 10 (October 1998): 387–89. http://dx.doi.org/10.1016/s0168-9525(98)01529-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
32

Joffe, Barry, and Paul Zimmet. "The Thrifty Genotype in Type 2 Diabetes: An Unfinished Symphony Moving to Its Finale?" Endocrine 9, no. 2 (1998): 139–42. http://dx.doi.org/10.1385/endo:9:2:139.

Full text
APA, Harvard, Vancouver, ISO, and other styles
33

Dowse, Gary K., Paul Z. Zimmet, Caroline F. Finch, and Veronica R. Collins. "Decline in Incidence of Epidemic Glucose Intolerance in Nauruans: Implications for the “Thrifty Genotype”." American Journal of Epidemiology 133, no. 11 (June 1, 1991): 1093–104. http://dx.doi.org/10.1093/oxfordjournals.aje.a115822.

Full text
APA, Harvard, Vancouver, ISO, and other styles
34

Kozlov, Andrey I., Svetlana A. Borinskaya, and Ekaterina D. Sanina. "APOE gene ε4/ε4 “thrifty” genotype and risk of metabolic disorders in the Uralic peoples." Ecological genetics 9, no. 2 (June 15, 2011): 17–23. http://dx.doi.org/10.17816/ecogen9217-23.

Full text
Abstract:
The prevalence of APOE gene ε4/ε4 genotype in the populations with various level of “westernization” is under the consideration. It is proposed that the populations with a high frequency of *ε4 undergoing “modernization transition” are in the most vulnerable state. These are the Eastern Finns and especially indigenous people of the North, who have a higher level of diseases of circulatory system than megacity residents.
APA, Harvard, Vancouver, ISO, and other styles
35

Bradley, Patrick J. "RE: “DECLINE IN INCIDENCE OF EPIDEMIC GLUCOSE INTOLERANCE IN NAURUANS: IMPLICATIONS FOR THE ‘THRIFTY GENOTYPE’”." American Journal of Epidemiology 136, no. 4 (August 15, 1992): 499–500. http://dx.doi.org/10.1093/oxfordjournals.aje.a116525.

Full text
APA, Harvard, Vancouver, ISO, and other styles
36

Sellayah, Dyan, Felino R. Cagampang, and Roger D. Cox. "On the Evolutionary Origins of Obesity: A New Hypothesis." Endocrinology 155, no. 5 (May 1, 2014): 1573–88. http://dx.doi.org/10.1210/en.2013-2103.

Full text
Abstract:
Obesity is an escalating threat of pandemic proportions, currently affecting billions of people worldwide and exerting a devastating socioeconomic influence in industrialized countries. Despite intensive efforts to curtail obesity, results have proved disappointing. Although it is well recognized that obesity is a result of gene-environment interactions and that predisposition to obesity lies predominantly in our evolutionary past, there is much debate as to the precise nature of how our evolutionary past contributed to obesity. The “thrifty genotype” hypothesis suggests that obesity in industrialized countries is a throwback to our ancestors having undergone positive selection for genes that favored energy storage as a consequence of the cyclical episodes of famine and surplus after the advent of farming 10 000 years ago. Conversely, the “drifty genotype” hypothesis contends that the prevalence of thrifty genes is not a result of positive selection for energy-storage genes but attributable to genetic drift resulting from the removal of predative selection pressures. Both theories, however, assume that selection pressures the ancestors of modern humans living in western societies faced were the same. Moreover, neither theory adequately explains the impact of globalization and changing population demographics on the genetic basis for obesity in developed countries, despite clear evidence for ethnic variation in obesity susceptibility and related metabolic disorders. In this article, we propose that the modern obesity pandemic in industrialized countries is a result of the differential exposure of the ancestors of modern humans to environmental factors that began when modern humans left Africa around 70 000 years ago and migrated through the globe, reaching the Americas around 20 000 years ago. This article serves to elucidate how an understanding of ethnic differences in genetic susceptibility to obesity and the metabolic syndrome, in the context of historic human population redistribution, could be used in the treatment of obesity in industrialized countries.
APA, Harvard, Vancouver, ISO, and other styles
37

Pijl, Hanno. "Reduced dopaminergic tone in hypothalamic neural circuits: expression of a “thrifty” genotype underlying the metabolic syndrome?" European Journal of Pharmacology 480, no. 1-3 (November 2003): 125–31. http://dx.doi.org/10.1016/j.ejphar.2003.08.100.

Full text
APA, Harvard, Vancouver, ISO, and other styles
38

Sharma, Arya M. "The thrifty-genotype hypothesis and its implications for the study of complex genetic disorders in man." Journal of Molecular Medicine 76, no. 8 (June 22, 1998): 568–71. http://dx.doi.org/10.1007/s001090050251.

Full text
APA, Harvard, Vancouver, ISO, and other styles
39

Reales, Guillermo, Diego L. Rovaris, Vanessa C. Jacovas, Tábita Hünemeier, José R. Sandoval, Alcibiades Salazar‐Granara, Darío A. Demarchi, et al. "A tale of agriculturalists and hunter‐gatherers: Exploring the thrifty genotype hypothesis in native South Americans." American Journal of Physical Anthropology 163, no. 3 (May 2, 2017): 591–601. http://dx.doi.org/10.1002/ajpa.23233.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

Poulsen, P., G. Andersen, M. Fenger, T. Hansen, S. M. Echwald, A. Volund, H. Beck-Nielsen, O. Pedersen, and A. Vaag. "Impact of Two Common Polymorphisms in the PPAR Gene on Glucose Tolerance and Plasma Insulin Profiles in Monozygotic and Dizygotic Twins: Thrifty Genotype, Thrifty Phenotype, or Both?" Diabetes 52, no. 1 (January 1, 2003): 194–98. http://dx.doi.org/10.2337/diabetes.52.1.194.

Full text
APA, Harvard, Vancouver, ISO, and other styles
41

Gosling, Anna L., Hallie R. Buckley, Elizabeth Matisoo-Smith, and Tony R. Merriman. "Pacific Populations, Metabolic Disease and ‘Just-So Stories’: A Critique of the ‘Thrifty Genotype’ Hypothesis in Oceania." Annals of Human Genetics 79, no. 6 (September 29, 2015): 470–80. http://dx.doi.org/10.1111/ahg.12132.

Full text
APA, Harvard, Vancouver, ISO, and other styles
42

Kozlov, A. I., S. A. Borinskaya, and E. D. Sanina. "The APOE gene ɛ4/ɛ4 “thrifty genotype” and risk of metabolic disorders in populations of the Ural region." Russian Journal of Genetics: Applied Research 2, no. 2 (April 2012): 135–40. http://dx.doi.org/10.1134/s2079059712020050.

Full text
APA, Harvard, Vancouver, ISO, and other styles
43

Dyck, Roland F., Helena Klomp, and Leonard Tan. "From “Thrifty Genotype” to “Hefty Fetal Phenotype”: The Relationship Between High Birthweight and Diabetes in Saskatchewan Registered Indians." Canadian Journal of Public Health 92, no. 5 (September 2001): 340–44. http://dx.doi.org/10.1007/bf03404975.

Full text
APA, Harvard, Vancouver, ISO, and other styles
44

Southam, L., N. Soranzo, S. B. Montgomery, T. M. Frayling, M. I. McCarthy, I. Barroso, and E. Zeggini. "Is the thrifty genotype hypothesis supported by evidence based on confirmed type 2 diabetes- and obesity-susceptibility variants?" Diabetologia 52, no. 9 (June 13, 2009): 1846–51. http://dx.doi.org/10.1007/s00125-009-1419-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
45

Albright, Julia W. "Interactions of Overweight, Poor Oral Health, and Stress Related to Chronic Disease in an Aging Population." Current Gerontology and Geriatrics Research 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/614814.

Full text
Abstract:
The prevalence of excess body mass (XBM), poor oral health (POH), and stress in a secluded population of aged (≥60 years) Hmong immigrants was surveyed. The findings were related to the prevalence of diabetes in the same population. Diabetes was associated separately with POH (OR 2.4; CL 1.3, 4.2) or with XBM (OR 2.5; CL 1.4, 4.8). The association of diabetes with the combination of XBM and POH was striking (OR 5.1; CL 3.4, 7.5); that apparent synergism has not been fully appreciated. We describe a mechanism that explains the synergism. The concept of “thrifty genotype” is a plausible explanation of XBM in the elderly Hmong immigrants and possibly the current older Laotian population. POH is common among elderly Laotians as it is in most developing countries. We conclude that synergism of XBM and POH significantly elevates the prevalence of diabetes among aging populations and probably other age groups as well.
APA, Harvard, Vancouver, ISO, and other styles
46

Li, Xiao, Xiubin Sun, Li Jin, and Fuzhong Xue. "Worldwide spatial genetic structure of angiotensin-converting enzyme gene: a new evolutionary ecological evidence for the thrifty genotype hypothesis." European Journal of Human Genetics 19, no. 9 (May 11, 2011): 1002–8. http://dx.doi.org/10.1038/ejhg.2011.66.

Full text
APA, Harvard, Vancouver, ISO, and other styles
47

Demidova, T. Yu, K. G. Lobanova, N. S. Shevtsova, T. N. Korotkova, and A. S. Kochina. "Influence of gut microbiota on the development of insulin resistance." Meditsinskiy sovet = Medical Council, no. 10 (June 18, 2022): 84–95. http://dx.doi.org/10.21518/2079-701x-2022-16-10-84-95.

Full text
Abstract:
Insulin resistance (IR) is an important problem of humanity, which leads to development of many metabolic disorders. Сurrently the pathogenic mechanism of the development of IR is not completely investigated. Nevertheless, there are some hypotheses explaining the development of this condition. These include such hypotheses as the hypothesis of thrifty genotype, thrifty phenotype, hormonal, stress, good and bad calories, chronic metabolic inflammation, microbiotic and integrated model suggested by Professor Rainer Straub. In this article, the microbiotic theory will be considered in detail, explaining the mechanism of the development of peripheral tissue insensitivity to insulin in dysbiosis due to amplification of transmission by proinflammatory molecules from the intestine to the bloodstream and activation of systemic inflammation, disruption of the “gut-brain-periphery” mechanism and impaired receptor interactions of active intestinal metabolites of the gut microbiota (GM) at the level of cells of metabolic organs. The value of this theory is that its factors affect all links in the pathogenesis of the development of IR, reflected in the integrated model of Professor Straub. In this review the influence of GM and metabolic processes of human body on the development of IR will be considered in detail, data from clinical studies about the influence of GM (its composition, active metabolites, individual bacterial strains) on the development of IR and the role of chronic metabolic inflammation in this process will also be presented. In addition, attention will be paid to bidirectional effects of GM and metformin, as well as to data from clinical studies on changes in GM in healthy people and people with IR under the influence of metformin and how GM affects the pharmacokinetics of this drug. The possibility of IR correction through the use of dietary fiber will also be considered.
APA, Harvard, Vancouver, ISO, and other styles
48

Gonzalez-Añover, P., E. Vigo, T. Encinas, L. Torres-Rovira, P. Pallares, E. Gomez-Izquierdo, R. Sanchez-Sanchez, F. Mallo, and A. Gonzalez-Bulnes. "Prepuberal evolution of plasma leptin levels in gilts of thrifty genotype (Iberian pig) and lean commercial crosses (Large White×Landrace)." Research in Veterinary Science 93, no. 1 (August 2012): 100–102. http://dx.doi.org/10.1016/j.rvsc.2011.08.006.

Full text
APA, Harvard, Vancouver, ISO, and other styles
49

Benyshek, Daniel C. "Type 2 Diabetes and Fetal Origins: The Promise of Prevention Programs Focusing on Prenatal Health in High Prevalence Native American Communities." Human Organization 64, no. 2 (May 26, 2005): 192–200. http://dx.doi.org/10.17730/humo.64.2.kk7y77qhna0819bj.

Full text
Abstract:
Recent diabetes research is challenging the longstanding emphasis on the primary role genes play in the type 2 diabetes epidemic among Native American and other high prevalence populations. Increasingly, “thrifty genotype” models are being reevaluated and modi?ed in order to accommodate experimental and epidemiological research that highlights the powerful effects of the prenatal environment in the development of the disorder. This body of research suggests that, especially in high-risk populations, diabetes may result initially from prenatal malnutrition followed by calorically adequate diets in adulthood, and then be propagated in subsequent generations via maternal hyperglycemia during pregnancy. The present paper highlights the recent research that is challenging the dominant genetic-predisposition model of diabetes, and then explores the promise of future community-based diabetes intervention strategies informed by this research. It suggests that prevention programs that focus on improved prenatal care have the best chance of signi?cantly reducing the incidence and prevalence of diabetes in high risk Native American communities, and explains why such programs are likely to enjoy improved community support and participation.
APA, Harvard, Vancouver, ISO, and other styles
50

Glossmann, H. H. "Pharmacology of vitamin D." Osteologie 20, no. 04 (2011): 299–303. http://dx.doi.org/10.1055/s-0037-1620006.

Full text
Abstract:
SummaryA main source of food for ancient humans (“hunter-gatherers”) was fresh meat. It contains much more 25(OH) vitamin D3 (25[OH]D3) than vitamin D3. It seems likely that in northern Europe, where vitamin D is in short supply during the extended winter season, evolutionary forces may have led to optimization of intestinal absorption of 25(OH)D3: excellent oral bioavailability (60 – 80 %) and little inter-individual variation. 25(OH)D3 could be considered the ideal oral “sunshine equivalent” for rapid and reliable restoration of an adequate vitamin D status e. g. in clinical situations. Unless biliary and pancreatic secretion or epithelial function in the small intestine is compromised, vitamin D3 in „pharmacological doses” is absorbed by 60 – 100 % as a „blind passenger” together with longchain fatty acids and cholesterol. The question is raised whether very low amounts of the vitamin (as in the diet) are absorbed by a more active (“second order”) mechanism. Experimental evidence obtained from cell culture systems indeed suggests that vitamin D3 can be taken up in part from enterocytes via the same complex, tightly regulated and saturable transport system as is e. g. cholesterol. The ezetimibe drug receptor NPC1L1 may play a role in this process. The Apolipoprotein Epsilon 4 genotype occurs in a north-south gradient in Europe. Allele frequencies are as high as 30 % in Finland and much lower, 5 %, around the Mediterranean Sea. The Epsilon 4 genotype may have been selected in the north because it enables more vitamin D to be obtained from food. The association of higher levels of 25(OH)D3 in humans with the Epsilon 4 genotype, together with evidence from knock-in mice, supports this hypothesis. It is possible, but as yet unproven, that this “lipid-thrifty” genotype is the cause of excess cardiovascular mortality sometimes observed in cohorts with high serum concentrations of 25(OH)D. Latitudinal gradients for mutations in the enzyme delta-7-dehydrocholesterol reductase (DHCR-7) suggest that similar evolutionary adaptations occurred for vitamin D synthesized in the skin following sun exposure.
APA, Harvard, Vancouver, ISO, and other styles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography