Abstract The aim of this study was to describe the characteristic features of weight management and lifestyle changes of people of working age at risk of type 2 diabetes. Seventy-four persons at high risk of type 2 diabetes, 33 men and 41 women, took part in the study. They attended group counselling sessions led by a dietician either at distance or face-to-face. There were 5 distance groups, with the counselling given by a dietician via a videoconferencing link to participants who met in the meeting room of their local health care centre. There were 6 personal groups where the dietician and the group participants met face-to-face at the same location. Each group had 5 to 9 participants. The following were used as study material: videotaped group discussions on the benefits and barriers of lifestyle changes at the beginning of the counselling process, weight management at the beginning and at the end of the process, and weight management and the preconditions and risk factors of successful weight management at the follow-up visit 1.5 years after the end of the process. In addition, study data were gathered before the first and last interventions and before the follow-up visit with a questionnaire sent to the subjects. The subjects were weighed at the beginning and at the end of the counselling process as well as at the follow-up visit. The video material was analysed using both inductive and deductive content analysis. The data were analysed also using SPSS 16.0 software for Windows. At the beginning of the counselling process, 68%, 9% and 14% of the subjects were at the contemplation, preparation and action stages, respectively, the corresponding percentages at the end of the counselling process being 24%, 33% and 40%. Forty subjects had made progress in their lifestyle change stage, 18 had remained where they had been, while 5 had regressed. One and a half year after the end of the counselling process, about half of the subjects were at the maintenance phase in terms of various lifestyle factors (restricting the amount of food, eating regular meals, increasing the intake of nutritional fibre, unsaturated fat and physical activity, restricting alcohol intake). Twenty-one subjects reported relapses, most often in terms of restricting the amount of food intake. Improved health and functional ability were seen as the benefit of lifestyle change. A change in lifestyle calls for effort and resources. The preconditions of successful weight management were one.s own actions, motivation and resources. Weight management was made more difficult by lack of commitment to one’s own actions and lack of goals, self-discipline and motivation. The information obtained with the study may be utilised in developing interventions aimed at persons at risk of type 2 diabetes as well as their contents and methods. The results can also be made use of in improving the counselling skills of health-care students and professionals. / Tiivistelmä Tutkimuksen tarkoituksena oli kuvata tyypin 2 diabeteksen riskiryhmään kuuluvien työikäisten henkilöiden painonhallinnan ja elintapamuutoksen tunnuspiirteitä. Tutkimukseen osallistui 74 työikäistä tyypin 2 diabeteksen korkean riskin henkilöä. Tutkittavista 33 oli miehiä ja 41 naisia He osallistuivat ravitsemusterapeutin ryhmäohjaukseen joko etä- tai lähiryhmässä. Etäryhmiä oli 5. Niissä ohjaus toteutui siten, että ohjaaja oli videoneuvottelulaitteiden avulla yhteydessä ryhmäläisiin, jotka olivat kokoontuneet oman kuntansa terveyskeskuksen kokoustilaan. Lähiryhmiä oli 6. Niissä ohjaus toteutettiin siten, että ohjaaja ja ryhmäläiset olivat samassa tilassa. Kussakin ryhmässä oli 5–9 osallistujaa. Tutkimusaineistona käytettiin videoituja keskusteluaineistoja, joissa ryhmään osallistuneet kuvasivat elintapamuutoksen hyötyjä ja haittoja ohjausprosessin alussa, painonhallintatilannettaan ohjausprosessin alussa, lopussa ja seurantakäynnillä sekä painonhallinnan onnistumisen edellytyksiä ja riskitekijöistä seurantakäynnillä 1,5 vuotta ohjausprosessin päättymisen jälkeen. Lisäksi tutkimusaineistoa kerättiin ennen ensimmäistä ja viimeistä ohjauskertaa sekä ennen seurantakäyntiä tutkittaville lähetetyllä kyselyllä. Paino mitattiin ohjausprosessin alussa, lopussa ja seurantakäynnillä. Videoaineisto analysoitiin sekä induktiivisella että deduktiivisella sisällönanalyysilla. Aineiston analysoinnissa käytettiin myös SPSS 16.0 for Windows -ohjelmaa. Ohjausprosessin alussa tutkittavista 68 % oli harkintavaiheessa, 9 % valmistautumis- ja 14 % toimintavaiheessa ja ohjausprosessin lopussa 24 % oli harkinta-, 33 % valmistautumis- ja 40 % toimintavaiheessa. Tutkittavista 40 edistyi elintapamuutosvaiheessaan, 18 pysyi ennallaan ja 5 taantui. Puolentoista vuoden kuluttua ohjausprosessin päättymisestä noin puolet tutkittavista oli ylläpitovaiheessa jonkun elintavan suhteen (kuidun ja rasvan käyttö, ruokamäärä, ateriarytmi, liikunta, alkoholin käyttö). Repsahduksista raportoi 21 henkilöä. Niitä oli tapahtunut eniten ruokamäärän rajoittamisen suhteen. Elintapamuutoksen hyötynä nähtiin terveyden ja toimintakyvyn paraneminen. Elintapamuutos vaatii vaivannäköä ja voimavaroja. Painonhallinnan onnistumisen edellytyksiä olivat oma toiminta, motivaatio ja voimavarat. Sitoutumattomuus omaan toimintaan, tavoitteiden, itsekurin ja motivaation puute vaikeuttivat painonhallintaa. Tutkimuksen avulla saatua tietoa voidaan käyttää kehitettäessä tyypin 2 diabeteksen riskiryhmiin kuuluvien henkilöiden ohjauksen sisältöä ja menetelmiä. Tuloksia voidaan hyödyntää myös terveydenhuollon opiskelijoiden ja ammattihenkilöiden ohjaustaitojen kehittämisessä.

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Bakgrund: Diabetes typ 2 är en av västvärldens vanligaste folksjukdomar med direkt koppling till levnadsvanor och livsstil. Aktuell forskning visar att det finns goda möjligheter att förebygga insjuknande och utveckling av följdsjukdomar genom en hälsofrämjande livsstil. Primärvårdens distriktssköterskor har en viktig roll i det preventiva hälsoarbetet med att vägleda patienter till en hälsofrämjande livsstil. Syfte: Syftet med studien var att beskriva hur patienter med diabetes typ 2 upplever att genomföra hälsofrämjande livsstilsförändringar efter samtal med distriktssköterska i primärvården. Metod: Kvalitativ ansats med en beskrivande design har använts. Data samlades in genom semistrukturerade intervjuer med öppna frågor. I studien deltog 11 personer som haft diagnosen diabetes typ 2 i ett år eller mer och som kunde ge adekvata svar på frågor. Data analyserades med kvalitativ innehållsanalys. Huvudresultat: Patienterna beskrev betydelsen av kunskap som central för att nå en ökad förståelse och komma till insikt om livsstilens betydelse för blodglukosnivå och behandling och de upplevde att distriktssköterskan vid diabetesmottagningen fyllde en viktig funktion för att understödja den lärprocessen. Med en tydligare förståelse för situationen upplevde patienterna en ökad motivation till att genomföra hälsofrämjande livsstilsförändringar. Slutsats: Patienterna upplevde att kunskap och information hade stor betydelse för att uppnå en god blodglukoskontroll och en hälsofrämjande livsstil. Det är betydelsefullt att primärvård och distriktssköterskor satsar resurser på rådgivning, blodglukoskontroller och egenvårdsutbildningar för att stärka förmåga och motivation till en hälsofrämjande livsstil. / Background: Type 2 diabetes is a global public health problem directly linked to poor diet and lack of exercise. Effective approaches are available to prevent type 2 diabetes and to prevent disease-related complications, and taking a lifestyle perspective is essential. Primary care nurses have an important role with disease-prevention when leading patients towards a health-promoting lifestyle. Purpose: To describe how patients with type 2 diabetes experience making changes towards a health-promoting lifestyle, after meeting with primary care nurses. Method: A descriptive design with a qualitative approach was used. Data was collected through interviews with 11 patients with a semi-structured guide of open-ended questions. Inclusion criteria for the study were as follows: patients diagnosed with type 2 diabetes for one year or longer who were able to respond adequately to questions. Data was analysed with qualitative content analysis. Main Results: Patients described knowledge regarding the disease as a key aspect when gaining understanding related to the bearing of lifestyle on blood sugar level and treatment of type 2 diabetes. They described that the primary care nurse had an important role in providing data and offering support whilst helping the patients taking a lifestyle perspective on diabetes. With a broader understanding of the condition the patients experienced an increase in motivation when making changes towards a health-promoting lifestyle. Conclusion: Patients described knowledge and understanding regarding the disease as key aspects to achieve a good blood glucose level and a health-promoting lifestyle. It is of great importance that primary care nurses invest resources in counselling, blood glucose monitoring and self-management education to increase motivation and ability of self-management and to support a health-promoting lifestyle.

Type 2 diabetes mellitus (T2DM) is an increasing global health concern, currently affecting an estimated 382 million individuals. There is no cure for T2DM and the search for new and improved treatments is ongoing. Presently, various pharmacological regimens are available to treat T2DM, but with varied success. Thousands of traditional herbs are also used to treat T2DM, but mainly without scientific validation. The aim of this study was to assess the polyphenolic content, antioxidant capacity, as well as in vitro toxicity and hypoglycaemic activity of a commercial ‘antidiabetic’ tea mixture (Diabetea) and its individual constituents: Achillea millefolium L. (Yarrow), Agathosma betulina Bartl. & Wendl. (Buchu), Salvia officinalis L. (Sage), Taraxacum officinalis L. (Dandelion), Thymus vulgaris L. (Thyme), Trigonella foenum-graecum L. (Fenugreek) and Urtica urens L. (Nettle). All herbs were tested as crude extracts, prepared using hot water (HW) and dichloromethane (DCM). The total polyphenolic content of each extract was determined using the Folin-Ciocalteau and aluminium trichloride methods. The non-cellular antioxidant activity was assessed using 2,2-azinobis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS) and 1,1-diphenyl-2-picrylhydrazyl (DPPH) methods. The cell-based antioxidant activity was measured against p-chloranil-induced generation of reactive oxygen species (ROS) in Ea.hy926 cells, using the fluorescent dye, 2',7'-dichlorfluorescein-diacetate (DCFH-DA). The effect of each extract on the viability of C2C12 myotubes, Ea.hy926 endothelial cells and human lymphocytes (HL) was determined using sulforhodamine B (SRB). The in vitro hypoglycaemic activity was assessed against α-amylase and α-glucosidase activity using 3,5-dinitrosalicylic acid (DNSA) and p-nitrophenyl-α-D-glucopyranoside (p-NPG), respectively. The type of inhibition exerted on these enzymes was determined using the Michaelis-Menten enzyme kinetics model, expressed as mixed, competitive, non-competitive and uncompetitive. Glucose uptake activity was measured using the 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-D-glucose (2-NBDG) fluorescent analogue. T. vulgaris and S. officinalis had the highest amount of polyphenols of all extracts tested. The HW extracts of T. vulgaris and S. officinalis showed significant (p < 0.05) cell-free antioxidant activity and cell-based radical scavenging activity. In addition, U. urens (HW) also limited cell-based ROS generation (p < 0.05). The Diabetea extracts presented with poor antioxidant activities, of which some had a pro-oxidant effect on Ea.hy926 cells. The positive linear relationship between antioxidant activity and polyphenolic content was shown to be dependent on the solvent type used. All of the DCM extracts had low antioxidant activity and polyphenolic content. None of the extracts produced < 50% cell density at the concentrations tested (1.3 - 20 μg/mℓ). In general, the DCM extracts showed a greater decrease in cell density than the HW extracts. The Ea.hy926 cells were the least affected by the extracts in terms of decreased cell density. The DCM extract of U. urens inhibited α-amylase activity in a mixed manner, which was comparable to the percentage inhibition exerted by the commercial drug, acarbose. Both the HW and DCM extracts of U. urens caused a significant (p < 0.05) increase in glucose uptake into C2C12 myotubes. The HW extract of T. vulgaris had a significant (p < 0.05) inhibitory activity against α-glucosidase (mixed). It also caused the uptake of glucose into C2C12 myotubes, which was significantly (p <0.05) more active than insulin. S. officinalis (DCM extract) also inhibited α-glucosidase activity (p < 0.05) in a mixed manner. Its HW extract displayed potent hypoglycaemic potential by causing glucose uptake into C2C12 myotubes, which was more significant (p < 0.05) than the activity of the positive control, insulin. The DCM extract of A. betulina was active against α-glucosidase (non-competitive), which was comparable to the activity of acarbose. Its HW extract also showed a significant (p < 0.05) glucose uptake activity. Furthermore, the DCM extracts of T. officinalis, A. millefolium, Diabetea and HW extracts of T. foenum-graecum and T. officinalis also caused a significant (p < 0.05) increase in glucose uptake into C2C12 myotubes. This study provides evidence for the antidiabetic potential of T. vulgaris and S. officianlis, in terms of antioxidant capacity and potential to prevent of post-prandial hyperglycaemia and alleviate hyperglycaemia by mimicking the action of insulin. In addition, the organic preparation of U. urens is also a potent α-amylase inhibitor. All herbs tested in this study exerted some form of in vitro antidiabetic activity. The Diabetea mixture, as a traditional preparation, did not have a significant antidiabetic capacity. In vitro observations from this study do not support the use of Diabetea as an antidiabetic preparation and reveal that some of the individual extracts prove more efficacious than the herb mixture. / Dissertation (MSc)--University of Pretoria, 2014. / lk2014 / Pharmacology / MSc / Unrestricted

Le diabète de type 2 est aujourd'hui un réel problème de santé publique mondial. Il résulte d'un défaut de masse et/ou de fonction des cellules bêta pancréatiques. L'identification et la compréhension des mécanismes à l'origine de ces défauts permettrait de développer des stratégies pour restaurer la masse fonctionnelle de cellules bêta. Les hormones glucocorticoïdes (GC), hormones de stress et d'adaptation métaboliques, sont capables d'inhiber la sécrétion d'insuline mais leur mode d'action n'est pas encore entièrement compris. Récemment, la sérotonine, neurotransmetteur présent dans les cellules bêta, a été décrite comme étant à l'origine de l'augmentation de la masse bêta lors de la gestation et d'une modulation de la sécrétion d'insuline chez la souris. Dans ce contexte, nous avons voulu définir si les GC pouvaient moduler le système sérotonine des cellules bêta. Nous nous sommes alors intéressés aux enzymes de synthèse de la sérotonine Tph1 et Tph2. Nous avons pu montrer que l'expression des enzymes Tph1 et Tph2 était inhibée par les GC entrainant une diminution de la synthèse de la sérotonine. Ensuite nous avons confirmé que l'expression de Tph1 et 2 était stimulée par la prolactine mais aussi montré pour la première fois que ces enzymes étaient stimulées par l'exenatide-4, un analogue de GLP-1. Dans ces deux situations stimulantes, nous retrouvons un effet contre-régulateur des GC. Enfin, nous nous sommes intéressés au rôle de la sérotonine sur la fonction des cellules bêta. Nous avons pu mettre en évidence que la sérotonine est capable d'inhiber la sécrétion d'insuline par altération du flux calcique dans la cellule bêta pancréatique. En conclusion, nos résultats montrent que, au sein de la cellule bêta, le système sérotonine est une des cibles des GC, suggérant que la réduction de sérotonine puisse être un relais des effets des GC sur les cellules bêta. / Type 2 diabetes is now a real global public health problem. It results from a defect of mass and / or function of pancreatic beta cells. The identification and understanding of the mechanisms underlying these defects would help develop strategies to restore the functional beta cell mass. Glucocorticoid hormones (GC), hormones of stress and metabolic adaptation, can inhibit insulin secretion but their mode of action is not yet fully understood. Recently, the neurotransmitter serotonin present in the beta cells has been described as involved in the increase in beta-cell mass during gestation and a modulation of the insulin secretion in mice. In this context, we wanted to determine whether GC could modulate the serotonin system of beta cells. We focused on the enzymes required for serotonin synthesis Tph1 and 2. We could show that the expression of Tph1 and Tph2 1 and Tph2 enzyme was inhibited by GC causing a decrease in serotonin synthesis. We then confirmed the expression of Tph1 and 2 was stimulated by prolactin but also showed for the first time that these enzymes were stimulated by exenatide-4, a GLP-1. In these two stimulating situations, we found that GC exerts a counter-regulatory effect. Finally, we studied the role of serotonin on beta cell function. We were able to show that serotonin can inhibit the secretion of insulin by altering the calcium flux in the pancreatic beta cell. In conclusion, our results show that, within the beta cell, the serotonin system is one of GC target, suggesting that serotonin reduction can be a relay of the effects of GC on beta cells.

L’obésité est une pathologie multifactorielle qui contribue au développement de l’insulinorésistance (l’IR). De nos jours, même si de nombreux travaux ont permis de répondre à plusieurs questions relatives à la pathogenèse de l’IR, les mécanismes cellulaires et moléculaires qui sous-tendent la pathogenèse de l’IR ne sont pas encore complètement élucidés chez l’Homme. Deux hypothèses principales se sont dégagées de ces travaux.D’une part, certaines études suggèrent que le défaut primaire à l’origine de l’IR se trouverait au niveau du tissu adipeux, qui en libérant dans la circulation systémique des adipokines, des cytokines inflammatoires et des acides gras contribue au développement d’une inflammation et d’une hyperlipidémie systémique. Ces deux paramètres exercent des effets délétères sur la sensibilité à l’insuline des autres organes comme le muscle et le foie.D’autre part, le muscle étant l’organe gluco-régulateur par excellence en situation postprandiale, d’autres études le place au cœur de la physiopathologie de l’IR.Malgré ces controverses, aucune étude n’a à ce jour exploré simultanément l’inflammation et l’IR systémique /tissulaire dans le muscle et le tissu adipeux chez un même sujet.Dans ce contexte, l’objectif de ce travail de thèse était de mieux comprendre les mécanismes impliqués dans la mise en place de l’IR. Il s’inscrit dans le cadre d’un projet de recherche translationnel, qui compare dans une cohorte de femmes ménopausées, des sujets minces à des sujets obèses de grade I insulinosensibles (OIS) et insulinorésistants (OIR). Plusieurs paramètres systémiques et tissulaires (lipotoxicité, inflammation et activation du récepteur toll like receptor 4 (TLR4)) impliqués dans la physiopathologie de l’IR ont été analysés chez ces sujets.Les résultats de cette étude mettent en avant l’importance de l’activation des voies de l’immunité innée dans la régulation de la sensibilité à l’insuline. Ainsi, alors qu’aucune inflammation systémique n’est détectée, on observe une activation différentielle des voies de signalisation du récepteur TLR4 de l’immunité innée entre le tissu musculaire et le tissu adipeux des sujets OIR. La voie MyD88-dépendante qui est une voie pro-inflammatoire, est activée dans le muscle squelettique de ces sujets et est associée à une IR au sein de ce tissu. A l’inverse, la voie TRIF-dépendante qui est une voie anti-inflammatoire est activée au sein du tissu adipeux et permet le maintien de la sensibilité à l’insuline. Ce maintien de la réponse à l’insuline se fait grâce l’induction du système interféron et de l’enzyme anti-oxydante manganèse superoxyde dismutase (MnSOD).Dans ce travail, nous montrons d’une part, que le défaut de réponse à l’insuline musculaire se trouve au cœur de la physiopathologie de l’IR chez les sujets obèses de grade I. D’autre part, ces résultats mettent en exergue l’importance de la balance de régulation des voies de l’immunité innée « MyD88 » et « TRIF » dans le maintien de la sensibilité à l’insuline. / Obesity is a multifactorial disease promoting the development of insulin resistance (IR). Nowadays, cellular and molecular mechanisms underlying IR pathogenesis in humans are not fully understood although many studies have been attempted to improve our knowledge. Tow hypotheses arose from these researches.On one hand, several studies have led to the idea that a chronic inflammatory state combined with adipose tissue (AT) dysfunction could be the so-called “central mechanism” leading to IR. AT dysfunction is associated with increase in the release of inflammatory adipokines/cytokines and free fatty acid (FFA), leading to systemic inflammation and lipid overload. These latter parameters would have deleterious effects on diverse organs such as muscles and liver by affecting their insulin sensitivityOn the other hand, skeletal muscle (SM) is responsible for 80% of glucose uptake and metabolism in postprandial state and muscle failure in this function is often considered as the first defect causing IR.Interestingly, despite these controversies, in human, insulin sensitivity and the onset of inflammation have so far never been investigated simultaneously at systemic level and locally in SM and AT in the same individual.In this context, the aim of this thesis was to better understand the mechanisms involved in IR development in grade I obese subject. It is based on a translational research project that compares in a cohort of postmenopausal women, lean subjects with grade I obese insulin-sensitive (OIS) and insulin-resistant (OIR) subjects. Several systemic and tissue parameters (lipotoxicity, inflammation and toll like receptor 4 (TLR4) activation), involved in the IR pathophysiology were analyzed in these subjects.Our results highlight the importance of innate immunity pathways activation in the regulation of insulin sensitivity. Thus, while no inflammation was detected at the systemic level, there is a differential activation of innate immune TLR4 signaling pathways between muscle and AT of OIR subjects. The MyD88-dependent pathway, a pro-inflammatory pathway, is activated in their SM and is associated with IR in this tissue. Conversely, the TRIF-dependent pathway which is an anti-inflammatory pathway is activated in the AT thus maintaining insulin sensitivity in this tissue. This is supported by the induction of interferon system and the antioxidant enzyme manganese superoxide dismutase (MnSOD).In this work, we show that SM defect is the central mechanism which determines IR in grade I obese subject. We have also highlighted the importance of regulation of the balance between the two innate immunity pathways "MyD88" and "TRIF" in maintaining insulin sensitivity.

Background: Multiple lines of evidence implicate the insulin-like growth factor(IGF) group of proteins in human type 2 diabetes. The actions of IGF-I and IGF-IIare modulated through their interaction with IGF binding proteins. A holisticapproach to study the IGF system is preferable to analyses of individual proteininteractions as the inter-relationships between these proteins are complex. Inparticular, the associations of IGF-II and its associated binding proteins withcardiovascular risk have been inadequately studied. This study aimed to study indetail the genotype and phenotype interactions of the IGF system with longitudinalcardiovascular risk factor trends and phenotypic outcomes in type 2 diabetes.Methods: 1000 subjects of predominantly Caucasian origin from the SalfordDiabetes Cohort were studied. Measurements of IGF proteins (IGF-I, IGF-II,IGFBP-1, IGFBP-2 and IGFBP-3) were performed in 554 of these patients. 991Caucasian subjects were successfully genotyped for 76 single nucleotidepolymorphisms (SNPs) related to ten genes in the IGF system. In this project weanalysed associations of the studied SNPs with the measured IGF proteins as well aslongitudinal risk factor trends. In addition, the baseline concentrations of themeasured proteins were studied for associations with cardiovascular risk factortrends and vascular outcomes.Results: This project demonstrates for the first time that high serum IGF-IIconcentration at baseline predicts longitudinal increases in high-density lipoproteincholesterol. High baseline IGF-II was also observed to predict longitudinal weightloss. High baseline concentration of IGFBP-2 (which has a preferential associationof IGF-II over IGF-I) was associated with a number of favourable longitudinalcardiovascular risk trends like increased HDL cholesterol and decreased diastolicblood pressure. However high IGFBP-2 was also associated with deterioration inrenal function and increased all-cause and cardiovascular mortality. The IGF2 geneand the genes encoding IGFBP-2 and IGFBP-5 (proteins with IGF-II bindingaffinity) were also associated with longitudinal trends in renal function, bloodpressure and cholesterol concentration.Discussion: This study is the most detailed exploration to date of the genotype andphenotype interactions of the IGF system in a Caucasian population with type 2diabetes. Results from this study strongly hint that changes in IGF-II bioavailabilitymay influence inter-individual variations in cardiovascular risk. The precisebiological role of IGF-II merits clarification in future expression studies in renal,adipose and vascular tissues. Replication of significant results in an independentdiabetes cohort and measurement of other IGF binding proteins will be performed inthe next stage of this study.

Objectives: The EZSCAN is a non-invasive device that, by evaluating sweat gland function, may detect subjects with type 2 diabetes mellitus (T2DM). The aim of the study was to conduct a systematic review and meta-analysis including studies assessing the performance of the EZSCAN for detecting cases of undiagnosed T2DM. Methodology/Principal findings: We searched for observational studies including diagnostic accuracy and performance results assessing EZSCAN for detecting cases of undiagnosed T2DM. OVID (Medline, Embase, Global Health), CINAHL and SCOPUS databases, plus secondary resources, were searched until March 29, 2017. The following keywords were utilized for the systematic searching: type 2 diabetes mellitus, hyperglycemia, EZSCAN, SUDOSCAN, and sudomotor function. Two investigators extracted the information for meta-analysis and assessed the quality of the data using the Revised Version of the Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) checklist. Pooled estimates were obtained by fitting the logistic-normal random-effects model without covariates but random intercepts and using the Freeman-Tukey Arcsine Transformation to stabilize variances. Heterogeneity was also assessed using the I2 measure. Four studies (n = 7,720) were included, three of them used oral glucose tolerance test as the gold standard. Using Hierarchical Summary Receiver Operating Characteristic model, summary sensitivity was 72.0% (95%CI: 60.0%– 83.0%), whereas specificity was 56.0% (95%CI: 38.0%– 74.0%). Studies were very heterogeneous (I2 for sensitivity: 79.2% and for specificity: 99.1%) regarding the inclusion criteria and bias was present mainly due to participants selection. Conclusions: The sensitivity of EZSCAN for detecting cases of undiagnosed T2DM seems to be acceptable, but evidence of high heterogeneity and participant selection bias was detected in most of the studies included. More studies are needed to evaluate the performance of the EZSCAN for undiagnosed T2DM screening, especially at the population level.

Chronic low-grade inflammation has been implicated in the processes leading to the development of type 2 diabetes (T2D) and its progression. Non-Hispanic Blacks bear a disproportionate burden of T2D and are highly susceptible to inflammation. This cross-sectional study assessed and compared the serum levels of established adipocytokines; interleukin-6 (IL-6), C-reactive protein (CRP), leptin, and novel adipocytokines; chemerin and omentin in Haitian and African Americans with and without T2D. The relationships of these adipocytokines with metabolic syndrome (MetS), anthropometric and HOMA2 measures by ethnicity and diabetes status were also assessed. Serum levels of IL-6, CRP, leptin, chemerin and omentin were determined by the ELISA method. HOMA2 measures were calculated for insulin sensitivity (HOMA2-IS) and insulin resistance (HOMA2-IR). Analyses of available data for 230 Haitian Americans and 241 African Americans (240 with and 231 without T2D) for the first study showed that Haitian Americans with and without MetS had lower levels of IL-6 and CRP compared to African Americans with and without MetS (P Ethnic-specific diabetes intervention and treatment programs must be designed to target Haitian Americans and African Americans as separate unique groups, in order to reduce the burden of T2D among the non-Hispanic Black community. Further research is needed to gain better understanding of the role of inflammation and T2D in this population.

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