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Dissertations / Theses on the topic 'Energy and glucose homeostasis'

Author: Grafiati

Published: 28 September 2024

Last updated: 31 July 2025

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1

Forsyth, Robert J. "The contribution of astrocyte glycogen to brain energy homeostasis." Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361387.

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2

Burke, Luke Kennedy. "Neurocircuitry underlying serotonin's effects on energy and glucose homeostasis." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708592.

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3

Matthäus, Dörte. "The role of CADM1 in energy and glucose homeostasis." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2014. http://dx.doi.org/10.18452/16905.

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Mehr als 300 Millionen Menschen sind weltweit von Diabetes betroffen, die Mehrheit davon leidet an Typ-2-Diabetes. Typ-2-Diabetes ist durch eine Insulinresistenz charakterisiert, welche meistens durch Übergewicht und Adipositas verursacht wird. Diese Insulinresistenz kann zunächst durch eine erhöhte pankreatische Insulinsekretion kompensiert werden, jedoch können langfristig die pankreatischen beta-Zellen den erhöhten Insulinbedarf nicht mehr decken. Dies verursacht einen starken Anstieg der Blutglucosespiegel und stellt den Beginn der Typ-2-Diabetes Erkrankung dar. Neben genetischen Veränderu

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4

Wang, Xun. "IRF3 is a Critical Regulator of Adipose Glucose and Energy Homeostasis." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10537.

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Obesity is associated with a state of chronic inflammation, which is believed to contribute to insulin resistance. We previously identified interferon regulatory factor 3 (IRF3) as an anti-adipogenic transcription factor with high expression in adipocytes. Because IRF3 is known to drive expression of pro-inflammatory genes in immune cells, we hypothesized that it may also promote inflammation and insulin resistance in adipocytes. Consistent with our expectations, we found that the expression of inflammatory genes in adipocytes was induced by IRF3 overexpression, while knockdown of IRF3 had the

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5

Hall, Jessica Ann. "Thyroid Hormone and Insulin Metabolic Actions on Energy and Glucose Homeostasis." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11663.

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Faced with an environment of constantly changing nutrient availability, mammals have adapted complex homeostatic mechanisms to maintain energy balance. Deviations from this balance are largely corrected through a concerted, multi-organ effort that integrates hormonal signals with transcriptional regulatory networks. When these relationships are altered, as with over-nutrition and insulin resistance, metabolic disease ensues. Here, I present data concerning two distinct transcriptional pathways--one for thyroid hormone (TH) and one for insulin--that confer hormone responsiveness on metabolic ge

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6

Rahman, S. A. "Investigating the role of gut hormones in energy and glucose homeostasis." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1417078/.

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Obesity is associated with type-2 diabetes mellitus. Gut hormones are peptides secreted in response to nutrient intake that act to regulate food intake, energy and glucose homeostasis. Thus, alterations in gut hormone abundance and/or signalling can contribute to the development of the obese and T2DM phenotype. The incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic hormone augment glucose-mediated insulin secretion. Peptide YY is released from the gut post-prandially and acts primarily as a satiety signal. Recently studies have highlighted a role for PYY in regulati

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7

Stump, Madeliene. "The role of brain PPAR[gamma] in regulation of energy balance and glucose homeostasis." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/6000.

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The Peroxisome Proliferator-Activated Receptor gamma (PPARγ), a master regulator of adipogenesis, has been shown to influence energy balance through its actions in the brain rather than in the adipose tissue alone. Deletion of PPARγ in mouse brain results in resistance to weight gain in response to high fat diet. Activation of PPARγ leads to change in the firing pattern of melanocortin system neurons (POMC and AgRP), which are critical for energy homeostasis. To determine the effects of modulation of brain PPARγ on food intake and energy expenditure we generated a novel transgenic mouse model

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8

Aatsinki, S. M. (Sanna-Mari). "Regulation of hepatic glucose homeostasis and Cytochrome P450 enzymes by energy-sensing coactivator PGC-1α". Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526208053.

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Abstract Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is a master regulator of energy metabolism and mitochondrial biology in high-energy cell types and tissues. The regulation of PGC-1α is versatile, and both transcriptional and post-transcriptional mechanisms play major roles. External stimuli affect PGC-1α-regulation which in turn adapts cellular signals to meet them. For example, conditions like fasting and diabetes mellitus (DM) are known to activate PGC-1α expression in the liver, resulting in enhanced de novo glucose production, gluconeogenesis. In the present st

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9

Eftychidis, Vasileios. "Elucidating the principal role of cholecystokinin neurons of the ventromedial hypothalamic nucleus in energy homeostasis." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:906a0aa6-847a-43b8-a527-458252aca825.

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The central nervous system (CNS) has a crucial role in the maintenance of energy homeostasis by orchestrating a plethora of signals from peripheral organs about the state of energy stores and the current energy intake needed to match energy expenditure. These signals converge into the hypothalamic regions and its complex local circuitry. CNS-derived cholecystokinin (CCK) is acting at central level to modulate energy balance by regulating the neuronal activity of hypothalamic neuronal populations that regulate food intake, energy storage and consumption. Moreover, our recent published work iden

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10

Birkenfeld, Andreas L. [Verfasser]. "The role of natriuretic peptides in the regulation of energy metabolism, lipid- and glucose homeostasis / Andreas L. Birkenfeld." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1035182424/34.

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11

Meyer, Cornelius [Verfasser], and Rey Adriana [Akademischer Betreuer] del. "Effects of interleukin-1 on glucose uptake and energy homeostasis in lymphocytes / Cornelius Meyer ; Betreuer: Adriana del Rey." Marburg : Philipps-Universität Marburg, 2020. http://d-nb.info/1224046765/34.

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12

Matthäus, Dörte [Verfasser], Thomas [Akademischer Betreuer] Sommer, Mathias [Akademischer Betreuer] Treier, and Susanne [Akademischer Betreuer] Klaus. "The role of CADM1 in energy and glucose homeostasis / Dörte Matthäus. Gutachter: Thomas Sommer ; Mathias Treier ; Susanne Klaus." Berlin : Humboldt Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2014. http://d-nb.info/104785273X/34.

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13

Weigt, Carmen. "Impact of estradiol, estrogen receptor subtype-selective agonists and genistein on energy homeostasis." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-127919.

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The prevalence of obesity is dramatically increasing and thus constitutes a major risk factor for developing chronic diseases such as type 2 diabetes, dyslipidemia, cardiovascular diseases, and certain forms of cancer. High-caloric nutrition and a lack of physical activity are the main contributing factors for this global epidemic. Estrogen receptors (ERs) are recognized to be involved in many processes related to the control of energy homeostasis. In my studies, I investigated the impact of estrogens (17beta-estradiol (E2)) on energy homeostasis. Special emphasis was given to the effects of t

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14

Hillier, Sarah Elizabeth. "The effects of fluctuations in oestrogen and progesterone during the menstrual cycle on glucose homeostasis, energy balance, exercise and premenstrual syndrome." Thesis, Oxford Brookes University, 2014. https://radar.brookes.ac.uk/radar/items/95a77132-ec7c-487b-8dde-11f3b7f57b2f/1/.

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It is widely accepted that the loss of sex hormones after the menopause is strongly linked with cancer, insulin resistance and obesity, with variations in sex hormone concentrations being responsible in part, for the differences reported in energy metabolism and glycaemic control between genders. As such a greater understanding of the effects that oestrogen and progesterone may have on women's health and their potential long term consequences is required. This thesis reports evidence of three studies investigating the effects of oestrogen and progesterone during the menstrual cycle on glucose

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15

Qian, Yanrong. "Internalization of Extracellular ATP in Cancer Cells and Development of New Generations of Anticancer Glucose Transport Inhibitors." Ohio University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1416411921.

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16

Troke, Rachel Clare. "A medical bypass : can the manipulation of gut hormone levels replicate the favourable effects on energy and glucose homeostasis seen following gastric bypass surgery?" Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/47922.

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The obesity crisis has reached epidemic proportions. Medical therapies are few and far between, offering only modest benefit, with maximal weight loss at one year in the region of 5-6%. Gastric bypass surgery and specifically Roux-en-Y gastric bypass (RYGB) is the only obesity treatment which has shown a marked and sustained weight loss, with initial remission of diabetes in up to 75% of patients. An increase in the post-prandial secretion of satiety gut hormones glucagon-like peptide-1 (GLP-1), peptide tyrosine-tyrosine (PYY) and oxyntomodulin (OXM) following gastric bypass may mediate these

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17

Chretien, Chloé. "Un nouvel acteur dans la détection hypothalamique du glucose : les canaux Transient Receptor Potential Canonical (TRPC)." Thesis, Dijon, 2015. http://www.theses.fr/2015DIJOS027/document.

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L’hyperglycémie est détectée et intégrée au niveau de l’hypothalamus médio-basal (MBH) qui inhibe la prise alimentaire et déclenche la sécrétion d’insuline. Le MBH renferme des neurones spécialisés gluco-sensibles (GS) qui détectent directement ou indirectement des variations de la concentration extracellulaire en glucose. Dans une première étude, nous suggérons que la détection indirecte du glucose par les neurones GS hypothalamiques repose sur la libération d’endozépines par les astrocytes, un gliotransmetteur connu pour inhiber la prise alimentaire en réponse à l’hyperglycémie. Nous travaux

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18

Desmoulins, Lucie. "Détection hypothalamique du glucose chez le rat soumis à un régime gras enrichi en saccharose : rôle de la dynamique mitochondriale et des espèces actives de l'oxygène d'origine mitochondriale." Thesis, Dijon, 2016. http://www.theses.fr/2016DIJOS024/document.

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L’hypothalamus participe au contrôle de l’homéostasie énergétique en détectant les signaux circulants tels que le glucose. L’hypothalamus médiobasal (MBH) en particulier, est capable de détecter l’hyperglycémie afin d’initier des réponses physiologiques adaptées, comme par exemple la sécrétion d’insuline via le système nerveux autonome (par un contrôle vagal). Notre équipe a récemment montré que la détection du glucose nécessite la production d’espèces actives de l’oxygène d’origine mitochondriale (mROS), fortement dépendante de la dynamique mitochondriale (fusion et fission). Récemment, l’étu

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19

Allard, Camille. "Les astrocytes et la détection hypothalamique du glucose : rôle métabolique et implication des connexines astrocytaires." Phd thesis, Université de Bourgogne, 2012. http://tel.archives-ouvertes.fr/tel-00935261.

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L'hypothalamus est fortement impliqué dans la régulation nerveuse de l'homéostasie énergétique. Il existe dans cette structure des neurones spécialisés (gluco-sensibles) qui détectent notamment l'hyperglycémie puis déclenchent des réponses adaptées comme le maintien de la glycémie, en stimulant la sécrétion d'insuline ou encore le rassasiement. Les astrocytes sont suspectés de participer à la détection neuronale du glucose. Dans l'ensemble du cerveau, il existe un couplage métabolique entre astrocytes et neurones. Le lactate, issu de la métabolisation du glucose par les astrocytes, est transpo

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20

Devère, Mélodie. "Découverte et caractérisation de nouveaux réseaux neuronaux peptidergiques gouvernant l'homéostasie énergétique et glucidique." Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMR031.

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La progression alarmante des épidémies d’obésité et de diabète à l’échelle mondiale fait du traitement de ces maladies un enjeu majeur de santé publique. Afin de développer de nouvelles approches thérapeutiques pour lutter contre la « Diabésité », il est crucial de comprendre l’étiologie de ces affections. Des recherches récentes mettent en lumière le rôle clé des réseaux neuronaux hypothalamiques dans la régulation de l’homéostasie énergétique et glucidique par le cerveau. Dans ce contexte, cette thèse visait à déterminer le rôle de deux systèmes neuropeptidergiques, le système 26RFa/GPR103 e

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21

Cham, Chee Wee. "Glucose homeostasis in rat liver transplantation." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309095.

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22

Ste, Marie Linda. "Role of norepinephrine in glucose homeostasis /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/9258.

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23

BonDurant, Lucas Donald. "Regulation of glucose homeostasis by FGF21." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6060.

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Fibroblast Growth Factor 21 (FGF21) is an endocrine hormone derived from the liver that exerts pleiotropic effects on the body to maintain overall metabolic homeostasis. During the past decade, there has been an enormous effort to understand the physiological roles of FGF21 in regulating metabolism and to identify the mechanism for its potent pharmacological effects to reverse diabetes and obesity. Through both human and rodent studies, it is now evident that FGF21 is dynamically regulated by nutrie

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24

Ng, Natasha Hui Jin. "The role of glucose-6-phosphatase catalytic domain in glucose homeostasis." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:1e5fc469-d474-45e8-9a6b-6b56d1cd3b77.

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Over the past decade, there has been unprecedented increase in the number of genetic loci associating with type 2 diabetes (T2D) risk and related glycemic traits, thanks to advances in sequencing technologies and access to large sample sizes. Identification of associated genetic variants across the frequency spectrum can provide valuable insight into disease pathophysiology. However, the translation into biological insights has been slow often due to uncertainties over the underlying effector transcripts. G6PC2/ABCB11 is one locus characterised by common non-coding variants that are strongly a

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25

Johnstone, Helen C. "Glucose homeostasis in fasting children with endocrinopathies." Thesis, University of Newcastle upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424085.

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26

Sabatini, Paul Vincent. "The role of NPAS4 in glucose homeostasis." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/58381.

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Type 2 diabetes is characterized by hyperglycemia associated with reduced insulin secretion from pancreatic beta cells and impaired insulin sensitivity at peripheral target tissues. There is a growing body of evidence that supports the importance of bHLH-PAS domain transcription factors in promoting beta cell function. With the recent identification of neuronal PAS domain protein 4 (NPAS4) within the central nervous system, studies were undertaken to determine whether NPAS4 is expressed in beta cells, how its expression is regulated in response to changing environmental signals and uncover the

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27

Sundbom, Maj. "Novel pharmaceutical approaches to regulate glucose homeostasis." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-743-6/.

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28

Mészáros, Gergő. "CaMK1D controls β-cell mass and glucose homeostasis". Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ035.

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Le diabètes mellites de type 2 (T2DM) est caractérisé par une hyperglycémie provenant d’une dérégulation de la sécrétion d’insuline combinée avec une altération de l’action de l’insuline. CaMK1D est un nouveau gène identifié, dont le rôle reste à explorer. Dans l’étude exposée ici, j’ai montré que CaMK1D a un effet majeur sur la régulation du glucose. J’ai observé une réduction exceptionnelle des taux de glucose sanguins à jeun, ce qui entraine une amélioration globale de la tolérance au glucose. Les souris mutantes montrent une augmentation conséquente dans les niveaux sanguins d’insuline. Le

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29

Baggio, Laurie L. "The role of incretin hormones in glucose homeostasis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ59004.pdf.

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30

Steiler, Tatiana L. "Kinase cascades in the regulation of glucose homeostasis /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-201-2/.

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31

Larson, Kara L. "Regulation of Glucose Homeostasis by the PHLPP1 Phosphatase." UKnowledge, 2014. http://uknowledge.uky.edu/biochem_etds/17.

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Type 2 diabetes mellitus is a metabolic disease that affects one in ten people in the United States. It is caused by a combination of genetics and lifestyle factors. Disease progression begins with insulin resistance in peripheral tissues followed by pancreatic beta-cell failure. The mechanisms behind disease progression are not completely understood. PH domain leucine rich repeat protein phosphatase 1 (PHLPP1) is a known regulator of Akt and other members of the AGC kinase family. Akt has been established to play a role in numerous metabolic signaling pathways, including insulin action. It is

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32

Chen, Mimi Zhu. "The effect of bariatric surgery on glucose homeostasis." Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.665171.

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Bariatric surgery is very effective at inducing weight loss and diabetes resolution in morbidly obese patients. Whether WL or increased incretin response is the crucial factor in normalising diabetes is still debatable. This thesis work prospectively investigated how bariatric surgery affected insulin action and beta-cell function in patients with morbid obesity and type 2 diabetes. Understanding these can help us to optimise diabetes treatments in patients with morbid obesity. I first discussed how obesity affects insulin sensitivity and beta-cell function, evidences that bariatric surgery is

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33

Flechner, Lawrence Martin. "Role of the CREB pathway in glucose homeostasis /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3129937.

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34

Shipley, Timothy I. "The Role of VMN Glucose-Sensitive Neurones in the Control of Glucose Homeostasis." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511846.

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35

Osundiji, Mayowa Azeez. "Hypothalamic glucose sensing plays a critical role in the control of glucose homeostasis." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612423.

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36

Smith, Kirsty Louise. "Metabolic hormones and energy homeostasis." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411789.

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37

Neary, Nicola Marguerite. "Gut hormones and energy homeostasis." Thesis, Imperial College London, 2007. http://hdl.handle.net/10044/1/7152.

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38

Pears, John Stuart. "Glucose-6-phosphatase : its structure, function and regulation in relation to blood glucose homeostasis." Thesis, University of Edinburgh, 1993. http://hdl.handle.net/1842/20100.

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Hepatic glucose-6-phosphatase (G6Pase) catalyses the final step in blood glucose production by the liver. It is a multicomponent system: the catalytic subunit is on the luminal surface of the endoplasmic reticulum membrane; there are transport proteins for glucose-6-phosphate, inorganic phosphate and glucose across the ER membrane; and there is a calcium-binding stabilising protein associated to the catalytic subunit. In fasted and diabetic humans (and rat models) kinetic analysis has shown that the capacity of the glucose-6-phosphate transport protein is the rate-limiting step in G6Pase activ

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Krishnan, Binu. "Hypothalamic and autonomic responses to change in glucose homeostasis." Thesis, Exeter and Plymouth Peninsula Medical School, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544012.

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Abrahamsson, Niclas. "On the Impact of Bariatric Surgery on Glucose Homeostasis." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-276381.

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Obesity has grown to epidemic proportions, and in lack of efficient life-style and medical treatments, the bariatric surgeries are performed in rising numbers. The most common surgery is the Gastric Bypass (GBP) surgery, with the Biliopancreatic diversion with duodenal switch (DS) as an option for the most extreme cases with a BMI>50 kg/m2. In paper I 20 GBP-patients were examined during the first post-operative year regarding the natriuretic peptide, NT-ProBNP, which is secreted from the cardiac ventricles. Levels of NT-ProBNP quickly increased during the first post-surgery week, and later

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Kindel, Tammy Lyn. "The Effects of Duodenal-jejunal Bypass on Glucose Homeostasis." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1280778030.

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Stevens, Joseph R. "The Effects of Low Dose Endotoxin on Glucose Homeostasis." Diss., Virginia Tech, 2014. http://hdl.handle.net/10919/64849.

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Obese individuals present with an increased inflammatory tone as compared to healthy, normal-weight individuals, which is associated with insulin resistance. One factor hypothesized to contribute to increased inflammation in obese and diabetic states is elevated blood endotoxin levels, also known as metabolic endotoxemia. In healthy rodents (non-obese and insulin sensitive), there is evidence that blood endotoxin levels fluctuate over the course of the day with elevations in the post-prandial state that return to baseline levels in the post-absorptive state. High-fat feeding in these animals a

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Hawke, Zoe Belinda. "Ventromedial hypothalamic neurones in energy homeostasis." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495608.

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The processes that control energy homeostasis are extremely complex and involve /nteractions between peripheral organs, the hypothalamus and the brainstem, as well as inputs from sensory and reward centres of the brain. Researchers have come a long way in recent years in elucidating the networks that control energy balance, but recent transgenic models have shown that over-emphasis may have been put on the arcuate nucleus Research is now shifting to extra-arcuate sites'including the ventromedial nucleus (VMN) which, unlike characterised in terms of its cellular phenotypes.

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Levi, Jasna. "The role of leptin in the regulation of glucose homeostasis." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/26267.

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The fat derived hormone leptin plays a crucial role in the normal maintenance of body weight and energy expenditure, as well as glucose homeostasis. Low doses of exogenous leptin administered to leptin deficient ob/ob mice are able to reverse the hyperinsulinemia and hyperglycemia without altering body composition. As leptin has the ability to directly suppress insulin secretion from ß-cells, we hypothesise that in the absence of leptin signalling, unregulated insulin secretion leads to hyperinsulinemia which in turn leads to increased adipogenesis and insulin resistance, ultimately culminat

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Kaur, Achint. "The role of sterol 12α- hydroxylase (Cyp8b1) in glucose homeostasis". Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/46516.

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Hawdon, Jane Melinda. "Metabolic adaptation and disordered blood glucose homeostasis in the neonate." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240735.

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Markkula, Silja Pauliina. "Hypothalamic hydrogen peroxide signalling in the control of glucose homeostasis." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609384.

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Castro, Acosta Monica Lizzette. "Beneficial effects of blackcurrant and apple polyphenols on glucose homeostasis." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/beneficial-effects-of-blackcurrant-and-apple-polyphenols-on-glucose-homeostasis(228bad46-5f9c-40be-b7d5-018445aaf7f4).html.

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Epidemiological evidence and randomised controlled trials suggests that dietary patterns with high intakes of fruit and vegetables are associated with reduced risk of cardiovascular disease (CVD) and type 2 diabetes (T2D). Frequent elevated excursions in postprandial glucose concentrations are thought to increase risk of T2D, therefore dietary strategies to control chronic postprandial hyperglycaemia would strengthen efforts to reduce the risk for T2D. Fruit polyphenols are dietary constituents that might help to delay glucose absorption following a carbohydrate-containing meal or beverage and

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Alkhalidy, Hana Awwad. "Flavonol kaempferol in the regulation of glucose homeostasis in diabetes." Diss., Virginia Tech, 2016. http://hdl.handle.net/10919/82485.

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Diabetes mellitus is a major public health concern. Although the accessible novel drugs, techniques, and surgical intervention has improved the survival rate of individuals with diabetes, the prevalence of diabetes is still rising. Type 2 diabetes (T2D) is a result of chronic insulin resistance (IR) and loss of β-cell mass and function. Therefore, the search for naturally occurring, low-cost, and safe compounds that could enhance insulin sensitivity and protect functional β-cell mass can be an effective strategy to prevent this disease. Kaempferol, a flavonol present in various medic

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Kent, Aysha S. "The role of ghrelin in energy homeostasis." Thesis, Imperial College London, 2006. http://hdl.handle.net/10044/1/11443.

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