Infection par le virus de l'herpès humain de type 8 (HHV8) et inflammation : implications dans le diabète de type 2 cétonurique.

Ketosis-Prone Diabetes (KPD) is a diabetes phenotype intermediate between type 1 and type 2 diabetes, frequently encountered in populations of African origin. This form of diabetes arouses some interest because of its clinical course marked in particular by restoring the initial impaired insulin secretion. Sobngwi et al. in 2008 established an association between HHV-8 virus and KPD in African population living in France. Nowhere else has the study been replicated. The objective of this thesis was to investigate the potential association between HHV-8 infection and KPD; then evaluate the impact of HHV-8 infection on the inflammatory profile of type 2 diabetes phenotypes. The study is based on African patients living in Africa consecutively admitted for hyperglycemic decompensation (Fasting blood glucose≥2,5g/l) at the National Obesity Centre of the Yaounde Central Hospital. More specifically, the issue was:• study the frequency of non-immune ketosis-prone diabetes (KPD);• investigate the association between HHV8 and KPD;• investigate whether HHV-8 infection is associated with an inflammatory profile that may participate in diabetes phenotypes.Was included in this study all diabetic patients old more than 18 years with acute diabetes with syndrome cardinal and ketonuria (KPD1), those who presented with an acute inaugural cardinal syndrome and diabetes ketonuria and in remission for more than three months and without ketonuria at baseline (KPD2), and those with type 2 diabetes experienced without ketonuria (T2D). Was excluded from the study all patient with stigmata of autoimmunity of type 1 A diabetes, diabetes "MODY", endocrinopathy, pancreatic disease or an autoimmune diabetes.Among all participants admitted, we collected clinical data (weight, height, BMI, waist to hip ratio, blood pressure, and the percentage of fat) and levies fasting were made (serum and peripheral blood mononuclear cells) for biological testing: glyceamia by glucose oxidase, HbA1c by HPLC, lipid profile by enzymatic methods, the insulin and C-peptide concentrations by electrochemiluminescence, anti-HHV8 antibodies by immunofluorescence, HHV8 viral DNA by real-time PCR, and markers of inflammation by Luminex. HOMA-β and HOMA-IR indices were used to assess insulinsecretion and insulinsensitivity respectively. Serological markers of inflammation investigated were : TNF-α, MCP-1, IL-8, MIP-1β, MIP-1α and VEGF...Le Ketosis-Prone Diabetes (KPD) est un phénotype de diabète intermédiaire entre le diabète de type 1 et le diabète de type 2, fréquemment rencontré chez le sujet d’origine noire africaine. Cette forme de diabète suscite un intérêt certain de par son évolution clinique marquée notamment par la restauration de l’insulinosécrétion initialement altérée. Sobngwi et coll. en 2008 ont établi une association entre le virus HHV8 et le KPD chez des sujets Africains vivant en France. Nulle part ailleurs l’étude n’a été reproduite. L’objectif de cette thèse était de rechercher la potentielle association entre l’infection à HHV8 et le KPD ; puis d’évaluer l’impact de l’infection à HHV8 sur le profil inflammatoire des phénotypes du diabète de type 2. L’étude s’appuie sur une population de patients Africains vivant en Afrique admis consécutivement pour une décompensation hyperglycémique (glycémie à jeun≥2,5g/l) au Centre National d’Obésité de l’Hôpital Central de Yaoundé. Plus spécifiquement, il était question de :•étudier la fréquence du diabète non auto-immun à tendance cétosique (KPD); •étudier l’association entre le virus HHV8 et le KPD;•rechercher si l’infection à HHV8 est associée à un profil inflammatoire pouvant participer aux phénotypes de diabète. Etait inclus dans l’étude tout patient diabétique âgé de plus de 18 ans présentant un diabète aigu avec syndrome cardinal et cétonurie (KPD1), ceux ayant présenté un diabète inaugural aigu avec syndrome cardinal et cétonurie et en rémission depuis plus de trois mois et sans cétonurie à l’inclusion (KPD2), et ceux présentant un diabète de type 2 connu sans cétonurie (DT2). Etait exclu de l’étude tout patient présentant des stigmates d’auto-immunité du diabète de type 1 A, un diabète « MODY », une endocrinopathie, une maladie du pancréas, ou un diabète de type auto-immun. Chez l’ensemble des participants admis, nous avons collecté les données cliniques (le poids, la taille, l’IMC, le rapport tour de taille sur tour de hanche, la pression artérielle, et le pourcentage de graisse) et des prélèvements à jeun ont été effectués (sérum et cellules mononuclées du sang périphérique) pour les analyses biologiques : la glycémie par glucose oxydase, l’HbA1c par HPLC, les paramètres du profil lipidique par des methodes enzymatiques, les concentrations d’insuline et de peptide-C par électrochimiluminescence, les anticorps anti-HHV8 par immunofluorescence, l’ADN viral HHV8 par PCR en temps réel, et les marqueurs de l’inflammation par le Luminex. Les indices HOMA-β et HOMA-IR ont été utilisés pour évaluer l’insulinosécrétion et la sensibilité à l’insuline respectivement. Les marqueurs sérologiques de l’inflammation recherchés étaient : TNF-α, MCP-1, IL-8, MIP-1β, VEGF et MIP-1α..

Seasonality in diabetes in Yaounde, Cameroon: a relation with precipitation and temperature

Abstract Background Diabetes is a growing health concern in developing countries, with Cameroon population having an estimated 6% affected. Of note, hospital attendees appear to be increasing all over the country, with fluctuating numbers throughout the annual calendar. The aim of the study was to investigate the relationship between diabete hospitalization admission rates and climate variations in Yaounde. Methods A retrospectively designed study was conducted in four health facilities of Yaounde (Central Hospital, University teaching hospital, Biyem-Assi and Djoungolo District Hospitals), using medical records from 2000 to 2008. A relationship between diabetes (newly diagnosed diabetes patients or decompensated diabetics) hospitalization admissions and climate variations was determined using the “2000–2008” national meteorological database (precipitation and temperature). Results The monthly medians of precipitation and temperature were 154mm and 25 °C, respectively. The month of October received 239mm of precipitation. The monthly medians of diabetic admissions rates (newly diagnosed or decompensated diabetes patients) were 262 and 72 respectively. October received 366 newly diagnosed diabetics and 99 decompensated diabetics. Interestingly, diabetic hospitalization admissions rates were higher during the rainy (51 %, 1633/3232) than the dry season, though the difference was non-significant. The wettest month (October) reported the highest cases (10 %, 336/3232) corresponding to the month with the highest precipitation level (239mm). Diabetes hospitalization admissions rates varied across health facilities [from 6 % (189/3232) in 2000 to 15 % (474/3232) in 2008]. Conclusion Diabetes is an important epidemiological disease in the city of Yaounde. The variation in the prevalence of diabetes is almost superimposed to that of precipitation; and the prevalence seems increasing during raining seasons in Yaoundé

Fasting insulin sensitivity indices are not better than routine clinical variables at predicting insulin sensitivity among Black Africans: a clamp study in sub-Saharan Africans

BACKGROUND: We aimed to evaluate the predictive utility of common fasting insulin sensitivity indices, and non-laboratory surrogates [BMI, waist circumference (WC) and waist-to-height ratio (WHtR)] in sub-Saharan Africans without diabetes. METHODS: We measured fasting glucose and insulin, and glucose uptake during 80/mU/m2/min euglycemic clamp in 87 Cameroonians (51 men) aged (SD) 34.6 (11.4) years. We derived insulin sensitivity indices including HOMA-IR, quantitative insulin sensitivity check index (QUICKI), fasting insulin resistance index (FIRI) and glucose-to-insulin ratio (GIR). Indices and clinical predictors were compared to clamp using correlation tests, robust linear regressions and agreement of classification by sex-specific thirds. RESULTS: The mean insulin sensitivity was M =10.5+/-3.2mg/kg/min. Classification across thirds of insulin sensitivity by clamp matched with non-laboratory surrogates in 30-48% of participants, and with fasting indices in 27-51%, with kappa statistics ranging from 0.10 to 0.26. Fasting indices correlated significantly with clamp (/r/=0.23-0.30), with GIR performing less well than fasting insulin and HOMA-IR (both p <0.02). BMI, WC and WHtR were equal or superior to fasting indices (/r/=0.38-0.43). Combinations of fasting indices and clinical predictors explained 25-27% of variation in clamp values. CONCLUSION: Fasting insulin sensitivity indices are modest predictors of insulin sensitivity measured by euglycemic clamp, and do not perform better than clinical surrogates in this population

Human herpes virus type 8 infection : implications in Ketosis prone type 2 diabetes

Le Ketosis-Prone Diabetes (KPD) est un phénotype de diabète intermédiaire entre le diabète de type 1 et le diabète de type 2, fréquemment rencontré chez le sujet d’origine noire africaine. Cette forme de diabète suscite un intérêt certain de par son évolution clinique marquée notamment par la restauration de l’insulinosécrétion initialement altérée. Sobngwi et coll. en 2008 ont établi une association entre le virus HHV8 et le KPD chez des sujets Africains vivant en France. Nulle part ailleurs l’étude n’a été reproduite. L’objectif de cette thèse était de rechercher la potentielle association entre l’infection à HHV8 et le KPD ; puis d’évaluer l’impact de l’infection à HHV8 sur le profil inflammatoire des phénotypes du diabète de type 2. L’étude s’appuie sur une population de patients Africains vivant en Afrique admis consécutivement pour une décompensation hyperglycémique (glycémie à jeun≥2,5g/l) au Centre National d’Obésité de l’Hôpital Central de Yaoundé. Plus spécifiquement, il était question de :• étudier la fréquence du diabète non auto-immun à tendance cétosique (KPD); • étudier l’association entre le virus HHV8 et le KPD;• rechercher si l’infection à HHV8 est associée à un profil inflammatoire pouvant participer aux phénotypes de diabète. Etait inclus dans l’étude tout patient diabétique âgé de plus de 18 ans présentant un diabète aigu avec syndrome cardinal et cétonurie (KPD1), ceux ayant présenté un diabète inaugural aigu avec syndrome cardinal et cétonurie et en rémission depuis plus de trois mois et sans cétonurie à l’inclusion (KPD2), et ceux présentant un diabète de type 2 connu sans cétonurie (DT2). Etait exclu de l’étude tout patient présentant des stigmates d’auto-immunité du diabète de type 1 A, un diabète « MODY », une endocrinopathie, une maladie du pancréas, ou un diabète de type auto-immun. Chez l’ensemble des participants admis, nous avons collecté les données cliniques (le poids, la taille, l’IMC, le rapport tour de taille sur tour de hanche, la pression artérielle, et le pourcentage de graisse) et des prélèvements à jeun ont été effectués (sérum et cellules mononuclées du sang périphérique) pour les analyses biologiques : la glycémie par glucose oxydase, l’HbA1c par HPLC, les paramètres du profil lipidique par des methodes enzymatiques, les concentrations d’insuline et de peptide-C par électrochimiluminescence, les anticorps anti-HHV8 par immunofluorescence, l’ADN viral HHV8 par PCR en temps réel, et les marqueurs de l’inflammation par le Luminex. Les indices HOMA-β et HOMA-IR ont été utilisés pour évaluer l’insulinosécrétion et la sensibilité à l’insuline respectivement. Les marqueurs sérologiques de l’inflammation recherchés étaient : TNF-α, MCP-1, IL-8, MIP-1β, VEGF et MIP-1α...Ketosis-Prone Diabetes (KPD) is a diabetes phenotype intermediate between type 1 and type 2 diabetes, frequently encountered in populations of African origin. This form of diabetes arouses some interest because of its clinical course marked in particular by restoring the initial impaired insulin secretion. Sobngwi et al. in 2008 established an association between HHV-8 virus and KPD in African population living in France. Nowhere else has the study been replicated. The objective of this thesis was to investigate the potential association between HHV-8 infection and KPD; then evaluate the impact of HHV-8 infection on the inflammatory profile of type 2 diabetes phenotypes. The study is based on African patients living in Africa consecutively admitted for hyperglycemic decompensation (Fasting blood glucose≥2,5g/l) at the National Obesity Centre of the Yaounde Central Hospital. More specifically, the issue was:• study the frequency of non-immune ketosis-prone diabetes (KPD);• investigate the association between HHV8 and KPD;• investigate whether HHV-8 infection is associated with an inflammatory profile that may participate in diabetes phenotypes.Was included in this study all diabetic patients old more than 18 years with acute diabetes with syndrome cardinal and ketonuria (KPD1), those who presented with an acute inaugural cardinal syndrome and diabetes ketonuria and in remission for more than three months and without ketonuria at baseline (KPD2), and those with type 2 diabetes experienced without ketonuria (T2D). Was excluded from the study all patient with stigmata of autoimmunity of type 1 A diabetes, diabetes "MODY", endocrinopathy, pancreatic disease or an autoimmune diabetes.Among all participants admitted, we collected clinical data (weight, height, BMI, waist to hip ratio, blood pressure, and the percentage of fat) and levies fasting were made (serum and peripheral blood mononuclear cells) for biological testing: glyceamia by glucose oxidase, HbA1c by HPLC, lipid profile by enzymatic methods, the insulin and C-peptide concentrations by electrochemiluminescence, anti-HHV8 antibodies by immunofluorescence, HHV8 viral DNA by real-time PCR, and markers of inflammation by Luminex. HOMA-β and HOMA-IR indices were used to assess insulinsecretion and insulinsensitivity respectively. Serological markers of inflammation investigated were : TNF-α, MCP-1, IL-8, MIP-1β, MIP-1α and VEGF..

Metabolic effects of quail eggs in diabetes-induced rats: comparison with chicken eggs

Background: Quail eggs as a food item have recently been introduced into the diet of some Cameroonians. These eggs are being sold in local markets, but with many unfounded health claims. One claim is that quail eggs can reduce blood glucose levels in diabetics. It was therefore necessary to evaluate the effect of consuming quail eggs on blood glucose levels, lipid profiles, and oxidative stress parameters in diabetes-induced rats. Methods: Twenty Wistar rats weighing, on average, 250 g were divided into four groups of five rats each. Group 1 consisted of rats with normal blood glucose, and the other three groups (2, 3, and 4) consisted of diabetes-induced rats achieved by intravenous injection of streptozotocin. During 16 days, rats in groups 1 and 2 received distilled water; and rats in groups 3 and 4 received quail and chicken eggs, respectively, with gastroesophageal probe at a dose of 1 mL/200 g body weight. Fasting blood glucose levels were determined in all the groups on the 1st, 7th, 14th, and 17th days after induction of diabetes. On the 17th day, the fasting rats were sacrificed, and blood and liver samples were collected for biochemical analyses. Results: In 17 days, the consumption of quail and chicken eggs had no effect on blood glucose levels of diabetic rats. Total cholesterol levels were higher in groups 3 (75.59 mg/dL) and 4 (59.41 mg/dL) compared to group 2 (55.67 mg/dl), although these differences were not significant (all p>0.05). Triglyceride levels were significantly higher (p <0.05) in groups 3 (106.52 mg/dL) and 4 (109.65 mg/dL) compared to group 2 (65.82 mg/dL). Quail eggs had no effect on oxidative stress parameters (malondialdehyde, hydroperoxides, and catalase). Conclusions: The consumption of quail eggs by diabetic rats at the tested dose had no effect on blood glucose level and oxidative stress parameters and may have a negative effect on lipid profile

Diabetes mellitus and inflammation

Type 2 diabetes mellitus (T2DM) is increasingly common worldwide. Related complications account for increased morbidity and mortality, and enormous healthcare spending. Knowledge of the pathophysiological derangements involved in the occurrence of diabetes and related complications is critical for successful prevention and control solutions. Epidemiologic studies have established an association between inflammatory biomarkers and the occurrence of T2DM and complications. Adipose tissue appears to be a major site of production of those inflammatory biomarkers, as a result of the cross-talk between adipose cells, macrophages, and other immune cells that infiltrate the expanding adipose tissue. The triggering mechanisms of the inflammation in T2DM are still ill-understood. Inflammatory response likely contributes to T2DM occurrence by causing insulin resistance, and is in turn intensified in the presence of hyperglycemia to promote long-term complications of diabetes. Targeting inflammatory pathways could possibly be a component of the strategies to prevent and control diabetes and related complications