Introduction: Insulin Pump Therapy has gained worldwide acceptance for the treatment of Type 1 diabetes mellitus (T1D), offering a new method of insulin delivery, which circumvents the need for Multiple Daily Injections (MDI). It is thought to improve quality of life (QoL) by facilitating an increase in lifestyle flexibility, independence and glycaemic control (Scottish Intercollegiate Guidelines Network, 2010; National Institute for Clinical Excellence, 2008). These benefits have resulted in the National Health Service (NHS) Scotland pledging funding of at least £1million to deliver insulin pumps to under 18s (Scottish Government, 2012). Currently, investigations regarding the impact of Insulin Pump Therapy on QoL have resulted in conflicting findings (Barnard et al., 2007). This study aims to explore the impact of Insulin Pump Therapy on the QoL of children and adolescents, using Interpretative Phenomenological Analysis. Method: Eight participants with T1D, aged between 8 and 13 years and using an insulin pump, were recruited from the Glasgow Royal Hospital for Sick Children Diabetes Clinic. Each participant completed an in-depth interview, which explored their beliefs and attitudes towards Insulin Pump Therapy including its impact on their QoL. Results: Analysis of the transcripts led to the identification of six super-ordinate themes: ‘Physical Impact’, ‘Mood and Behaviour’, ‘Lifestyle Flexibility’, ‘Practicalities’, ‘Peer Reactions’, and ‘Support’. It is suggested that these six factors are not mutually exclusive and together inform the complexity of individuals’ experiences and the impact that the insulin pump has had on many aspects of their lives. These findings suggest a framework to help clinicians understand how young people with T1D perceive and conceptualise their treatment regimes. Conclusions: There was general agreement amongst participants that switching to Insulin Pump Therapy resulted in improvements to their QoL. Additional concerns were outlined but reportedly none of the participants regretted switching to an insulin pump.

Background: Diabetes mellitus type 1 (DM1) is the most common form of diabetes in children. Strict glycaemic control can increase the risk of hypoglycaemia, which is characterised by a number of unpleasant and often frightening symptoms. Fear of Hypoglycaemia (FOH) is thought to contribute to psychological distress and diabetes management, however little is known about parents’ experiences of FOH. The aim of this study was to explore parents’ experience of FOH and its impact on their engagement with intensive insulin therapy. Methods: This qualitative study was conducted and analysed utilising an Interpretative Phenomenological Analysis (IPA) approach. Purposive, volunteer sampling was used. Semi-structured interviews were conducted with 4 parents in the hospital setting. These were transcribed and analysed. Results: The results of this study suggest that FOH is a very salient topic for parents of children with DM1. Four super-ordinate themes emerged: parents’ internal experience, coping, family unit and school. FOH appears to be characterised by a range of emotional and psychological symptoms. Parents attempt to manage the condition and their experiences through a combination of emotion-focused and problem-focused coping strategies. The systemic challenges of diabetes and FOH were highlighted by parents’ worries about their child’s safety when under the care of others and the burden that this places on them.

Patients with diabetic renal disease develop elevated urinary albumin excretion rates [AER] and hypertension. Preliminary data from several groups suggest that diabetic patients handle transferrin, a protein similar in size and weight, in a different fashion from albumin. In the first part of this thesis I report the results of clinical studies of urinary transferrin excretion [TER] in diabetes mellitus. More than 80% type 1 [insulin dependent] diabetic patients have increased TER but less than 40% have increased AER. TER may be provoked by exercise in uncomplicated type 1 diabetes and the rise is proportionally far greater than that for AER. Newly diagnosed type 2 [non-insulin dependent] diabetic subjects have increased TER which falls with improved glycaemic control. Interventional studies with lisinopril, an angiotensin converting enzyme [ACE] inhibitor, in microalbuminuric and macroalbuminuric diabetic subjects show a reduction in TER independent of reduction in blood pressure. Data are presented suggesting a role for altered renal tubular function in TER in diabetes. The second part of the thesis examines the role of the system in the hypertension of diabetic renal disease. Patients with elevated AER have increased resting plasma renin activity. Those with uncomplicated diabetes show an exaggerated blood pressure reponse to exercise. ACE inhibition reduces blood pressure in hypertensive patients and AER in both hypertensive and normotensive patients.

This thesis describes investigations of the usage of unconventional therapeutic methods to treat diabetes mellitus, with particular reference to Asian patients. Findings suggest that usage of unconventional therapeutic methods may persist in diabetic patients regardless of their language, religious belief, ethnic and cultural background or psychological states and adherence. The thesis is presented in two parts. Study 1, a preliminary study, was conducted in Thailand. Groups of adults with diabetes mellitus, aged 17 - 70+ years, were studied to assess the extent to which unconventional therapeutic methods were used, and to examine the possibility that such usage is associated with their psychological states and unsatisfactorily feelings toward orthodox medicine. Data collection was achieved through a combination of well-established and well-evaluated questionnaires and a structured interview. A scale to assess attitudes to diabetes was found to be reliable in this sample, but scales to measure diabetes knowledge and treatment satisfaction were not. Study 2 was a study of British Indo-Asians in Foleshill, Coventry, England. The extent to which medicinal plants were used was explored and compared between two different cultural and religious backgrounds of adults with diabetes: (1) born in an Asian country and (2) born in England. The majority of participants were old with low educational background and income. A number of modifications were made to the structured interview used in study 1 to make it more appropriate for this sample. The two studies suggest that usage of medicinal plants is common among diabetics in Thailand and among British Indo-Asian diabetics born in an Asian country. Only a minority of users of medicinal plants in both countries were willing to discuss their usage of medicinal plants with their physicians. This could be because users believed that their physicians might not approve the usage of non-orthodox treatment. In Thailand, usage of medicinal plants was significantly associated with one factor - a lack of basic diabetes knowledge. In the study in England, a typical user was characterised as an Asian female born in an Asian country, who had a low income, used betel-nut, had a preferencef or a doctor's ethnicity, and had low treatment satisfaction and adherence scores.

Diabetes mellitus (DM) is associated with the compromised digestion of carbohydrates. This complication is described as exocrine pancreatic insufficiency. Whilst this causes malnutrition in patients and contributes to diabetic morbidity, the physiology and molecular biology leading to this state is not well defined. This disease-induced inability to digest foodstuffs could have many levels of regulation. Obvious candidates are ligand proteins involved in stimulating secretion, receptor defects, intracellular ion levels and post-receptor signal transduction encompassing transcription and translation. To address these points, the current studies aimed to characterise the effects of experimental type I DM upon both physiological and molecular events. The first study investigated the effects of cholecystokinin-octapeptide (CCK-8) and exogenous insulin on exocrine pancreatic amylase secretion in streptozotocin (STZ)- induced diabetic rats compared to healthy age-matched controls in vivo and in vitro. Seven - eight weeks after the induction of diabetes, animals were either anaesthetised for the study of in vivo exocrine secretion or humanely killed and pancreatic acinar cells isolated for the measurement of intracellular free calcium and magnesium concentrations ([Ca 2+ ]1 and [Mg2+ ]1), total protein, and amylase output employing the Phadebas method. For rats in both in vivo and in vitro studies, fasting blood glucose in control and diabetic rats was 73.3 ± 3.4 mg dl-1 (n = 44) and 380.0 ± 25.9 mg dl-1 (n = 27), respectively. Basal pancreatic juice flow rate in STZ-diabetic rats was significantly increased (P<0.001) whereas protein and amylase outputs were significantly decreased (P<0.001) compared to control rats. CCK-8 infusion (150 pmol kg -1 h-1 for 100 mm) resulted in marked elevations in flow rate as well as in protein and amylase secretion in control animals (P<0.05 compared with the corresponding basals). In contrast, in diabetic rats, CCK-8 evoked a small increase in flow rate, which was not significant when compared to basal. In these animals, CCK-8 stimulated the secretion of amylase and protein output, but the secretory rates were dramatically lower compared with those in control rats. Administration of insulin (1 U, I.P.) in healthy rats significantly increased pancreatic flow rate, amylase secretion, protein output and blood glucose levels in vivo compared to basal (P<0.05). Infusion of CCK-8 together with insulin (1 U) in control rats markedly potentiated pancreatic juice flow and amylase secretion. Pretreatment with atropine (0.2 mg kg-1, I.P.) abolished the effects of insulin on secretory parameters despite a similar reduction in glycaemia. In diabetic rats, insulin (4 U, I.P.) did not modify exocrine pancreatic secretion either alone or in combination with CCK-8. In vitro experiments revealed that either (ACh (10-8 – 10-4 M) or CCK-8 (10" - 10-8 M)) can evoke total amylase release which was elevated in healthy control pancreatic acinar cells compared to diabetic acinar cells. In contrast, 10-6 M insulin produced a significant increase (Pc0.05) in the amount of total amylase output in control acinar cells compared to diabetic acinar cells. Combining insulin (10-8 – 10-6 M) with either ACh or CCK-8 had little or no effect on total amylase release in both control and diabetic acinar cells. There were no significant differences among the groups in unstimulated [Ca2+]j and [Mg2+]i. However, the peak [Ca 2+ ]i induced by 10-8 M CCK-8 was depressed (P<0.05) in diabetic cells (275.3 ± 11.5 nM n = 8) compared to (359.7 ± 27.5 nM, n = 6) control cells. Similarly, CCK-8 significantly decreased (P<0.05) [Mg2 ']1 in diabetic acinar cells compared to control. On a molecular level, the gene encoding amylase was under transcriptional dysregulation. Healthy control animals had a significantly lower (P>0.05) crossing point value (8.54 ± 0.131. n = 8) compared to STZ-induced diabetic animals (17.96 ± 0.272, n = 7), respectively. On a protein level, those mediators controlling translation such as p70 S6K and 4E-BPI were present at significantly lower (P>0.05) relative concentrations, suggesting an impaired capacity for protein synthesis. Interestingly, the actual activity of these proteins as measured by phosphorylation was slightly increased. It is suggested that this is a cellular mechanism to counteract loss in transcription and/or translation of mRNA encoding these proteins. Protein ubiquitination was also elevated suggesting increased protein breakdown which could be responsible for pancreatic atrophy and net protein loss. The NFkβ protein widely implicated in tissue atrophy was actually lower in STZ-induced DM, and therefore probably does not contribute to pancreatic wasting. To conclude, the results indicate that DM-induced exocrine pancreatic insufficiency is associated with decreased levels of total protein output and amylase secretion and these changes may be in part be associated with derangements in cellular Ca2+ and Mg2+ homeostasis. Furthermore, transcription of the α-amylase gene is reduced suggesting a reduced protein level and thus capacity for stimulus-secretion coupling. Finally, there appears impaired protein translation and elevated ATP-dependent protreasome mediated protein breakdown in STZ-induced DM.

Στα πλαίσια της παρούσας διπλωματικής εργασίας σχεδιάστηκε και αναλύθηκε ένα μοντέλο ολοκληρωμένου συστήματος διαχείρισης ατόμων με Σακχαρώδη Διαβήτη (ΣΔ), κυρίως ατόμων με Σακχαρώδη Διαβήτη Τύπου 1 (ΣΔΤ1), κάνοντας χρήση δικτύων επικοινωνιών τηλεϊατρικής. Κατά την διάρκεια της σχεδίασης και ανάλυσης του συστήματος – μοντέλου λάβαμε υπόψη μας τις ανάγκες όλων των εμπλεκομένων χρηστών (διαβητικούς, οικείους τους, φροντιστές, ιατρούς) ενσωματώνοντας τα πιο πρόσφατα τεχνολογικά εργαλεία. Σκοπός του μοντέλου είναι α) η χρήση τεχνολογιών φιλικών προς τους εμπλεκόμενους χρήστες, β) η σχεδίαση και ανάλυση ενός συστήματος όπου τα άτομα με ΣΔ θα αποκομίζονται τα οφέλη των τεχνολογικών εξελίξεων χωρίς όμως να αλλάξει η υπάρχουσα φιλοσοφία της καθημερινότητάς τους και γ) η μελλοντική υλοποίηση του συστήματος, να αναβαθμίζει την ποιότητα ζωής των ατόμων αυτών, ενώ παράλληλα να ενισχύει το αίσθημα ασφάλειας. Το μοντέλο-σύστημα το οποίο προτείνουμε αποτελείται από τα ακόλουθα υποσυστήματα: α) Σύστημα Διαχείρισης Διαβητικών (ΣΔΔ), β) Εφαρμογή Κινητών Επικοινωνιών (ΕΚΕ) , ενώ συγχρόνως υποστηρίζεται από κατάλληλη πλατφόρμα επικοινωνίας για την τηλε-παρακολούθηση και την τηλε-διαχείριση των ατόμων με ΣΔ. Το ΣΔΔ συνιστάται να αποτελείται από i) κεντρική βάση δεδομένων, ii) εφαρμογή διαχείρισης δεδομένων από τους ιατρούς, iii) εφαρμογή διαχείρισης δεδομένων από το άτομο με ΣΔ και iv) από σύνολο διεπαφών διασύνδεσης του ΣΣΔ με τα υπόλοιπα υποσυστήματα. Οι μηχανισμοί που προτείνονται πρέπει να παρέχουν ακεραιότητα και ασφάλεια μεταφοράς και αποθήκευσης των δεδομένων, καθώς και των αποτελεσμάτων της επεξεργασίας τους. Το μοντέλο αναδεικνύει την δυνατότητα μέσω του προτεινόμενου συστήματος τα δεδομένα του διαβητικού, είτε μέσω του διαδικτύου, είτε του δικτύου κινητής τηλεφωνίας να μεταφέρονται, στο θεράποντα ιατρό. Ο ιατρός με τη βοήθεια κατάλληλων υπολογιστικών εργαλείων αναλύει τα δεδομένα του διαβητικού και πραγματοποιεί καίριες παρεμβάσεις για τη θεραπεία του ατόμου με ΣΔ. Οι παρεμβάσεις μπορεί να είναι από απλές, όπως η χρήση της σύριγγας ή η διαιτητική αγωγή, έως σύνθετες, όπως τροποποίηση της δόσης ινσουλίνης ή ακόμα γνωστοποίηση της ανάγκης για νοσηλεία. Όταν αυτές είναι διαθέσιμες, ενημερώνουν απευθείας τις εφαρμογές που αφορούν το άτομο με ΣΔ. Επίσης, το προτεινόμενο σύστημα θα υποστηρίζει τη θεραπευτική αγωγή των πασχόντων μέσω κατάλληλου υπολογιστικού μοντέλου, το οποίο με την βοήθεια προηγουμένων δεδομένων του διαβητικού εκτιμά τη βέλτιστη ρύθμιση της ινσουλίνης. Τελικώς, το σύστημα προτείνεται να ενημερώνει με συνέπεια και ασφάλεια τον ηλεκτρονικό ιατρικό φακέλου του ασθενούς με στοιχεία που εξασφαλίζουν την σωστή καθοδήγησή του, ενώ παράλληλα εξυπηρετούν μελλοντικές αναφορές. / In the course of this project an integrated Diabetes Management System for Diabetes Mellitus (DM) patients was designed and analyzed especially for those suffering from Diabetes Type I. While designing and analyzing this model-system the needs of all relevant users (DM patients, their families, carers and physicians) was taken into consideration and at the same time the most advanced technological tools were used. The main aim of the developed system was i) the use of user friendly technology, ii) the design of a system whose users will capitalize on the benefits offered by technology advances while their everyday life and habits remain unchanged, iii) the improvement of DM patients’ quality of everyday life, while at the same time offer an increased feeling of health security. The model-system, which is proposed comprises of the following components: i) Diabetes Management System (DMS), ii) Mobile Phone Application, while at the same time is supported by the appropriate telecommunication platform for the remote monitoring and management of diabetes patients. DMS consists of i) a central database system, ii) an application for patient data to be managed by physicians, iii) an application for patient data to be managed by the DM patients themselves and iv) a number of interfaces between the DMS and other subsystems. The proposed mechanisms must provide data integrity as well as secure transmission and storage of the data and its analysis results. Via this model-system ,the DM patient’s data is transmitted to the physician either via the website or via the mobile phone. The physician using the appropriate tools, analyses the data and issues to the point, early and efficient interventions in order to improve the individual’s health status. These interventions range from simple ones, such as how to use the syringe or follow a diet regime, to complex ones such as changing the insulin dosage or even alerting the patient that he/she requires medical attention. When available, they immediately update all the DM patient, relevant applications. Moreover the proposed system allows for the automatic support of the patient’s treatment using an appropriate computational model. This model, using historical patient data suggests the optimal insulin dosage. Finally, the system is suggested to support the secure and timely update of the patient electronic health record, by inserting on a continuous basis, with vital information that will help him/her with his disease guidance as well as in future reports.

Background: Regional adiposity and in particular central adiposity is associated with a hazardous metabolic profile, insulin resistance (IR), hypertension and increased cardiovascular mortality whilst gluteo-femoral fat (peripheral fat) is protective. Extreme phenotypes, especially those due to monogenic disorders, are experiments of nature, which have been pivotal in identifying genes involved in disease. The hypothesis tested in this thesis was that investigating individuals with monogenic causes of regional adiposity and IR would identify genes and physiological processes contributing to their phenotype. Methods: Two families with balanced translocations, sixty-nine patients with partial lipodystrophy and eight individuals with lipoma were investigated. Genetic investigations included mapping of balanced translocations using fluorescent in-situ hybridisation, DNA and cDNA sequencing and gene expression studies. In vivo investigations of adipose tissue included microdialysis and measurement of adipose tissue blood flow. Results: Genetic and physiological factors contributing to regional adipose tissue deposition and IR were identified in (1) individuals with lipodystrophy where mutations were identified in eleven families including one novel PPARG mutation V450M. Also a skinfold ratio was developed for the clinical diagnosis of partial lipodystrophy (2) a family with a balanced I translocation, IR and growth retardation, digenic disruption of INSR and CHN2 was identified, which accounted for the clinical phenotype (3) a family with a balanced translocation, central adiposity and peas associated with disruption of KIBRA (4) lipoma tissue relative to adjacent healthy subcutaneous tissue, where differential gene expression profiles were identified, we also demonstrated reduced metabolic flexibility and reduced lipolysis in lipoma relative to healthy adipose tissue despite no change in adipose tissue blood flow. Conclusion: Investigating individuals with extreme phenotypes and monogenic causes of regional adiposity and IR identified key genetic and physiological factors.

The global prevalence of type 2 diabetes (T2DM) and obesity is increasing, with obesity the most important predisposing factor contributing to the development of T2DM. Epidemiological and genetic evidence supports a major genetic component in both multifactorial and heterogeneous disorders. The identification of disease susceptibility genes in humans could greatly assist in the elucidation of underlying pathophysiological mechanisms and allow the development of more effective preventative and therapeutic strategies for these conditions. Three candidate genes, uncoupling proteins 2 and 3 (UCP2; UCP3) and calpain 10 (CAPN10), are proposed and the rationale for their selection discussed. Gene variants were identified in UCP2 and UCP3. These variants were tested for association with T2DM, obesity and intermediate quantitative traits in a South Indian population and family collection, and also a cohort of British obese case/control subjects. No variant was associated with T2DM. However, investigations revealed positive associations with a UCP2 3'UTR 45bp Ins/Del and a novel UCP3 promoter variant (-55C/T) with variation in body mass (BMI) and fat distribution (WHR) respectively. The results support the view that uncoupling proteins may influence weight gain and hence progression to obesity/T2DM. A significant correlation with plasma leptin levels and the UCP2 Ins/Del variant might indicate one potential mechanism whereby weight could be modulated by uncoupling proteins. A linkage study in affected sibling pairs of North European descent, was negative for the putative T2DM susceptibility gene region, NIDDMI. In contrast, haplotypes of four sequence variants of a T2DM susceptibility gene (CAPN10) identified in this region positively associated with T2DM in a South Indian population. In conclusion, these investigations provide evidence that the three genes studied may contribute to susceptibility for development of T2DM or obesity. However, the findings are in agreement with the most likely genetic model for non-Mendelian complex diseases, that many genes are involved in determining susceptibility to disease with no single gene capable of determining the overall disease phenotype.

Σκοπός της μελέτης ήταν η διερεύνηση της σχέσης ανάμεσα στο μεταβολισμό του σιδήρου και το σακχαρώδη διαβήτη τύπου 2. Έτσι ο στόχος της παρούσης μελέτης ήταν διπλός. α) Να καθορισθεί η συχνότητα των μεταλλάξεων C282Y και H63D στον Ελληνικό πληθυσμό και να συγκριθεί με αυτήν άλλων χωρών και ταυτοχρόνως, να ελεγχθεί αν η συχνότητα των ανωτέρω μεταλλαγών είναι διαφορετική στους διαβητικούς τύπου 2 σε σχέση με το γενικό πληθυσμό και να γίνει συσχέτιση ανάμεσα στην ύπαρξη η όχι των μεταλλάξεων αυτών και σε δείκτες μεταβολισμού του σιδήρου όπως η φερριτίνη, ο σίδηρος, ο κορεσμός τρανσφερίνης. β) Να ελεγχθεί αν στους διαβητικούς τύπου 2, η συχνότητα της κληρονομικής αιμοχρωμάτωσης (ομοζυγώτες), όπως αυτή μπορεί να καθορισθεί με βάση το γονότυπο του γονιδίου HFE είναι αυξημένη σε σχέση με το γενικό πληθυσμό. Υλικό και μέθοδοι Αρχικά δείγμα 100 διαβητικών τύπου 2 και 100 ατόμων από το γενικό πληθυσμό ελέγθησαν για τις μεταλλάξεις του γονιδίου HFE C282Y και H63D με τη μέθοδο της PCR και RFLP. Στη συνέχεια μελετήθηκαν 500 διαβητικοί τύπου 2 και 423 μάρτυρες. Στα άτομα αυτά εκτιμήθηκε το φορτίο του οργανισμού σε σίδηρο (Σίδηρος ορού, ολική δεσμευτική ικανότητα σε σίδηρο, φερριτίνη) και καθορίστηκε ο γονότυπος αναφορικά με τις μεταλλάξεις C282Y και H63D με τη μέθοδο της PCR και RFLP. Αποτελέσματα- Συμπεράσματα 1. Η συχνότητα του αλληλομόρφου C282Y στον Ελληνικό πληθυσμό(0,0075) είναι χαμηλότερη των ατόμων Βορειοευρωπαικής καταγωγής και πλησιάζει αυτή ατόμων από περιοχές της νότιας Ευρώπης. Η συχνότητα του αλληλομόρφου H63D (0,115) είναι παρόμοια με αλλους πληθυσμούς. 2. Δεν ανευρέθη διαφορά στη συχνότητα των μεταλλάξεων C282Y και H63D ανάμεσα στην ομάδα των διαβητικών τύπου 2 και στο γενικό πληθυσμό. 3. Η παρουσία οποιασδήποτε από τις παραπάνω μεταλλάξεις στην ετερόζυγη μορφή συνεισφέρει στην αύξηση του φορτίου του οργανισμού σε σίδηρο. Αυτό βρέθηκε και στις δύο ομάδες. 4. Οι διαβητικοί τύπου 2 παρουσιάζουν μεγαλύτερο κορεσμό τρανσφερρίνης αίματος και υψηλότερα επίπεδα φερριτίνης συγκρινόμενοι με το γενικό πληθυσμό. Οι ανωτέρω δείκτες θα μπορούσαν να αντιπροσωπεύουν αυξημένο φορτίο του οργανισμού σε σίδηρο. 5. Λόγω της χαμηλής συχνότητας του αλληλομόρφου C282Y δεν κατέστη δυνατή η ανίχνευση ομοζυγωτών C282Y/ C282Y. / Several authors have suggested a positive association between diabetes type 2 and the C282Y and H63D mutations of the hereditary hemochromatosis gene but others have disputed it. There are also papers reporting an increased iron load in diabetes type 2 and possible associations with the pathogenesis of the disease. We performed therefore a study in 100 type 2 diabetics and 100 age and sex matched controls to assess the role of the C282Y and H63D mutations in the HFE gene as a risk factor for type 2 diabetes mellitus in Greece. We also evaluated the iron load in 500 diabetes type 2 patients and 423 age and sex matched controls. We did not find any differences in the allele frequencies of the above mutations between patients with diabetes type 2 and the controls. The allele frequencies are estimated to be 0.0075 for the C282Y and 0.115 for the H63D mutation. Subjects with at least one mutation (C282Y or H63D) had higher transferrin saturation compared to those with no such mutations. This seems to apply to both diabetics (49± 8,6 vs 44,5± 5,4, p<0,01) and control group (49,3± 7,3 vs 42,6± 3,3 p<0,01). Patients with diabetes type 2 have higher transferrin saturation compared to the general population. These differences were found among men (n=250, mean± SD 31,8+11 vs n=73, mean± SD 29,5+8, p=0,05) as well as among women (n=250, mean± SD 28.5+10 vs n=350, mean± SD 25.5+9.6, p=0.001). The present study is in concord with previous work reporting that type 2 diabetes patients have higher ferritin levels compared to controls.

No description available.