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Barry I. Joffe - One of the best experts on this subject based on the ideXlab platform.
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Distribution of autoantibodies to glutamic acid decarboxylase across the spectrum of Diabetes Mellitus seen in South Africa
Diabetic medicine : a journal of the British Diabetic Association, 2000Co-Authors: Vanessa R. Panz, W. J. Kalk, M. Zouvanis, Barry I. JoffeAbstract:SUMMARY Aims This study investigated the association between glutamic acid decarb- oxylase antibodies (GAD-AB) and Type 1, Type 2, pancreatic and Lipoatrophic Diabetes Mellitus (DM) in South African patients. Methods Four groups were selected: group A, 100 Black Type 1 DM patients (age at onset 35 years, BMI > 27 kg/m2 and controlled on oral hypoglycaemic agents for at least 1 year after presentation); group C, 10 patients of varying ethnicity with DM or impaired glucose tolerance secondary to chronic pancreatitis; group D, five patients of varying ethnicity with DM associated with total lipodystrophy. Fifty healthy Black control subjects were also studied (group E). Serum GAD-AB and random C-peptide levels were measured by radioimmunoassay. Results Mean C-peptide concentration was significantly lower in Type 1 DM patients than Type 2 DM patients (P 1 U/ml. Type 1 DM patients who were GAD-AB-positive did not differ from those who were GAD-AB-negative for age at onset, duration of DM or C-peptide concentrations. Conclusions Auto-immune beta-cell destruction has an important role in the pathogenesis of Type 1 DM amongst African patients. However, Type 2 African DM patients and other Diabetes subtypes are largely GAD-AB-negative.
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Free fatty acids and insulin levels--relationship to leptin levels and body composition in various patient groups from South Africa.
International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity, 1999Co-Authors: M-t Van Der Merwe, V. R. Panz, Barry I. Joffe, Gp Schlaphoff, Ip Gray, P Froguel, Nigel J. Crowther, Pn LönnrothAbstract:OBJECTIVE: To investigate the relationship between leptin concentrations, various metabolic indices and body composition in six different groups. DESIGN AND MEASUREMENTS: Anthropometric measurements, fasting plasma glucose, serum insulin, C-peptide, FFA and leptin levels were performed. In the obese and diabetic subjects, body composition was analysed with bioimpedance equipment and as a 5 level CT scan. SUBJECTS: Five Lipoatrophic Diabetes Mellitus (LDM) patients, five normal subjects (N), nine white and nine black obese women (WW, BW), and nine white and nine black diabetic women (DWW, DBW) were investigated after an overnight fast. RESULTS: In both ethnic groups there was a positive correlation between leptin and BMI (black group: ra 0.8; P< 0.0001, white group: ra 0.7, P< 0.002) and leptin and SC fat mass (black group: ra 0.6; P< 0.005, white group: ra 0.6; P< 0.004). CONCLUSIONS: Across the groups, there were positive linear correlations between leptin concentrations, BMI, SC fat mass and FFA levels. Leptin and FFA concentrations are higher and insulin levels lower in both groups of black women compared to the two groups of white women, despite a similar BMI and body fat mass. In the DBW the large increase in visceral fat mass may be indicative of a more complex relationship between compensatory insulin resistance, elevated FFA levels and leptin secretion.
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The thrifty genotype in type 2 Diabetes: an unfinished symphony moving to its finale?
Endocrine, 1998Co-Authors: Barry I. Joffe, Paul ZimmetAbstract:The basic premise of the thrifty gene hypothesis is that certain populations may have genes that determine increased fat storage, which in times of famine represent a survival advantage, but in a modern environment result in obesity and type 2 Diabetes. The concept finds support in a unique animal model (Psammomys obesus) as well as among high type 2 Diabetes susceptibility populations, such as North American Indians and South Pacific islanders. However, in some developing communities (e.g., Black South Africans) the thrifty phenotype hypothesis of perinatal malnutrition causing β-cell dysfunction seems a better explanation, but this remains a contentious issue. Several genes have already been identified as candidates for the thrifty genotype, including those encoding proteins of the insulin-signaling and leptin pathways, as well as intermediary fat metabolism. Particular interest lies in the peroxisome-proliferator activated receptors. An innovative approach might be to focus on the “mirror image” of the thrifty genotype—congenital Lipoatrophic Diabetes Mellitus, whose molecular defect remains enigmatic. We conclude that the genetic basis of the thrifty genotype probably derives from the multiplicative effects of polymorphisms at several sites mentioned above, rather than a single regulatory abnormality.
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improved glucose tolerance after effective lipid lowering therapy with bezafibrate in a patient with Lipoatrophic Diabetes Mellitus a putative role for randle s cycle in its pathogenesis
Clinical Endocrinology, 1997Co-Authors: V. R. Panz, J. R. Wing, Frederick J. Raal, Mary-anne Kedda, Barry I. JoffeAbstract:This report describes a patient with Lipoatrophic Diabetes Mellitus (LDM), which is a rare clinical syndrome characterized by lipoatrophy and severe insulin resistance. Although a genetic abnormality is suspected in the development of LDM, no functional mutations in key domains of the insulin receptor gene were detected. Therapy was directed primarily at decreasing the availability of non-esterified fatty acids (NEFA), and thereby improving glucose tolerance (Randle's cycle), by the administration of a lipid-lowering drug, bezafibrate. Serial changes in fasting levels of the hormones of glucose homeostasis and lipids were measured, as well as glucose and insulin responses to a 75-g oral glucose challenge at onset and following 3 and 6 months of fibrate therapy. Progressive reductions in the patient's levels of triglycerides and NEFA were paralleled by an improvement in beta-cell function, a decrease in insulin resistance, and the attainment of normal glucose homeostasis. We conclude that the pathogenesis of LDM may be related primarily to abnormal regulation of lipid, rather than glucose, metabolism.
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Improved glucose tolerance after effective lipid‐lowering therapy with bezafibrate in a patient with Lipoatrophic Diabetes Mellitus: a putative role for Randle’s cycle in its pathogenesis?
Clinical endocrinology, 1997Co-Authors: V. R. Panz, J. R. Wing, Frederick J. Raal, Mary-anne Kedda, Barry I. JoffeAbstract:This report describes a patient with Lipoatrophic Diabetes Mellitus (LDM), which is a rare clinical syndrome characterized by lipoatrophy and severe insulin resistance. Although a genetic abnormality is suspected in the development of LDM, no functional mutations in key domains of the insulin receptor gene were detected. Therapy was directed primarily at decreasing the availability of non-esterified fatty acids (NEFA), and thereby improving glucose tolerance (Randle's cycle), by the administration of a lipid-lowering drug, bezafibrate. Serial changes in fasting levels of the hormones of glucose homeostasis and lipids were measured, as well as glucose and insulin responses to a 75-g oral glucose challenge at onset and following 3 and 6 months of fibrate therapy. Progressive reductions in the patient's levels of triglycerides and NEFA were paralleled by an improvement in beta-cell function, a decrease in insulin resistance, and the attainment of normal glucose homeostasis. We conclude that the pathogenesis of LDM may be related primarily to abnormal regulation of lipid, rather than glucose, metabolism.
V. R. Panz - One of the best experts on this subject based on the ideXlab platform.
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Free fatty acids and insulin levels--relationship to leptin levels and body composition in various patient groups from South Africa.
International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity, 1999Co-Authors: M-t Van Der Merwe, V. R. Panz, Barry I. Joffe, Gp Schlaphoff, Ip Gray, P Froguel, Nigel J. Crowther, Pn LönnrothAbstract:OBJECTIVE: To investigate the relationship between leptin concentrations, various metabolic indices and body composition in six different groups. DESIGN AND MEASUREMENTS: Anthropometric measurements, fasting plasma glucose, serum insulin, C-peptide, FFA and leptin levels were performed. In the obese and diabetic subjects, body composition was analysed with bioimpedance equipment and as a 5 level CT scan. SUBJECTS: Five Lipoatrophic Diabetes Mellitus (LDM) patients, five normal subjects (N), nine white and nine black obese women (WW, BW), and nine white and nine black diabetic women (DWW, DBW) were investigated after an overnight fast. RESULTS: In both ethnic groups there was a positive correlation between leptin and BMI (black group: ra 0.8; P< 0.0001, white group: ra 0.7, P< 0.002) and leptin and SC fat mass (black group: ra 0.6; P< 0.005, white group: ra 0.6; P< 0.004). CONCLUSIONS: Across the groups, there were positive linear correlations between leptin concentrations, BMI, SC fat mass and FFA levels. Leptin and FFA concentrations are higher and insulin levels lower in both groups of black women compared to the two groups of white women, despite a similar BMI and body fat mass. In the DBW the large increase in visceral fat mass may be indicative of a more complex relationship between compensatory insulin resistance, elevated FFA levels and leptin secretion.
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Free fatty acids and insulin levels—relationship to leptin levels and body composition in various patient groups from South Africa
International Journal of Obesity, 1999Co-Authors: M-t Van Der Merwe, V. R. Panz, Nj Crowther, Gp Schlaphoff, Ip Gray, P Froguel, Bi Joffe, Pn LönnrothAbstract:OBJECTIVE: To investigate the relationship between leptin concentrations, various metabolic indices and body composition in six different groups. DESIGN AND MEASUREMENTS: Anthropometric measurements, fasting plasma glucose, serum insulin, C-peptide, FFA and leptin levels were performed. In the obese and diabetic subjects, body composition was analysed with bio-impedance equipment and as a 5 level CT scan. SUBJECTS: Five Lipoatrophic Diabetes Mellitus (LDM) patients, five normal subjects (N), nine white and nine black obese women (WW, BW), and nine white and nine black diabetic women (DWW, DBW) were investigated after an overnight fast. RESULTS: In both ethnic groups there was a positive correlation between leptin and BMI (black group: r =0.8; P
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improved glucose tolerance after effective lipid lowering therapy with bezafibrate in a patient with Lipoatrophic Diabetes Mellitus a putative role for randle s cycle in its pathogenesis
Clinical Endocrinology, 1997Co-Authors: V. R. Panz, J. R. Wing, Frederick J. Raal, Mary-anne Kedda, Barry I. JoffeAbstract:This report describes a patient with Lipoatrophic Diabetes Mellitus (LDM), which is a rare clinical syndrome characterized by lipoatrophy and severe insulin resistance. Although a genetic abnormality is suspected in the development of LDM, no functional mutations in key domains of the insulin receptor gene were detected. Therapy was directed primarily at decreasing the availability of non-esterified fatty acids (NEFA), and thereby improving glucose tolerance (Randle's cycle), by the administration of a lipid-lowering drug, bezafibrate. Serial changes in fasting levels of the hormones of glucose homeostasis and lipids were measured, as well as glucose and insulin responses to a 75-g oral glucose challenge at onset and following 3 and 6 months of fibrate therapy. Progressive reductions in the patient's levels of triglycerides and NEFA were paralleled by an improvement in beta-cell function, a decrease in insulin resistance, and the attainment of normal glucose homeostasis. We conclude that the pathogenesis of LDM may be related primarily to abnormal regulation of lipid, rather than glucose, metabolism.
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Improved glucose tolerance after effective lipid‐lowering therapy with bezafibrate in a patient with Lipoatrophic Diabetes Mellitus: a putative role for Randle’s cycle in its pathogenesis?
Clinical endocrinology, 1997Co-Authors: V. R. Panz, J. R. Wing, Frederick J. Raal, Mary-anne Kedda, Barry I. JoffeAbstract:This report describes a patient with Lipoatrophic Diabetes Mellitus (LDM), which is a rare clinical syndrome characterized by lipoatrophy and severe insulin resistance. Although a genetic abnormality is suspected in the development of LDM, no functional mutations in key domains of the insulin receptor gene were detected. Therapy was directed primarily at decreasing the availability of non-esterified fatty acids (NEFA), and thereby improving glucose tolerance (Randle's cycle), by the administration of a lipid-lowering drug, bezafibrate. Serial changes in fasting levels of the hormones of glucose homeostasis and lipids were measured, as well as glucose and insulin responses to a 75-g oral glucose challenge at onset and following 3 and 6 months of fibrate therapy. Progressive reductions in the patient's levels of triglycerides and NEFA were paralleled by an improvement in beta-cell function, a decrease in insulin resistance, and the attainment of normal glucose homeostasis. We conclude that the pathogenesis of LDM may be related primarily to abnormal regulation of lipid, rather than glucose, metabolism.
Mary-anne Kedda - One of the best experts on this subject based on the ideXlab platform.
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improved glucose tolerance after effective lipid lowering therapy with bezafibrate in a patient with Lipoatrophic Diabetes Mellitus a putative role for randle s cycle in its pathogenesis
Clinical Endocrinology, 1997Co-Authors: V. R. Panz, J. R. Wing, Frederick J. Raal, Mary-anne Kedda, Barry I. JoffeAbstract:This report describes a patient with Lipoatrophic Diabetes Mellitus (LDM), which is a rare clinical syndrome characterized by lipoatrophy and severe insulin resistance. Although a genetic abnormality is suspected in the development of LDM, no functional mutations in key domains of the insulin receptor gene were detected. Therapy was directed primarily at decreasing the availability of non-esterified fatty acids (NEFA), and thereby improving glucose tolerance (Randle's cycle), by the administration of a lipid-lowering drug, bezafibrate. Serial changes in fasting levels of the hormones of glucose homeostasis and lipids were measured, as well as glucose and insulin responses to a 75-g oral glucose challenge at onset and following 3 and 6 months of fibrate therapy. Progressive reductions in the patient's levels of triglycerides and NEFA were paralleled by an improvement in beta-cell function, a decrease in insulin resistance, and the attainment of normal glucose homeostasis. We conclude that the pathogenesis of LDM may be related primarily to abnormal regulation of lipid, rather than glucose, metabolism.
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Improved glucose tolerance after effective lipid‐lowering therapy with bezafibrate in a patient with Lipoatrophic Diabetes Mellitus: a putative role for Randle’s cycle in its pathogenesis?
Clinical endocrinology, 1997Co-Authors: V. R. Panz, J. R. Wing, Frederick J. Raal, Mary-anne Kedda, Barry I. JoffeAbstract:This report describes a patient with Lipoatrophic Diabetes Mellitus (LDM), which is a rare clinical syndrome characterized by lipoatrophy and severe insulin resistance. Although a genetic abnormality is suspected in the development of LDM, no functional mutations in key domains of the insulin receptor gene were detected. Therapy was directed primarily at decreasing the availability of non-esterified fatty acids (NEFA), and thereby improving glucose tolerance (Randle's cycle), by the administration of a lipid-lowering drug, bezafibrate. Serial changes in fasting levels of the hormones of glucose homeostasis and lipids were measured, as well as glucose and insulin responses to a 75-g oral glucose challenge at onset and following 3 and 6 months of fibrate therapy. Progressive reductions in the patient's levels of triglycerides and NEFA were paralleled by an improvement in beta-cell function, a decrease in insulin resistance, and the attainment of normal glucose homeostasis. We conclude that the pathogenesis of LDM may be related primarily to abnormal regulation of lipid, rather than glucose, metabolism.
Frederick J. Raal - One of the best experts on this subject based on the ideXlab platform.
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improved glucose tolerance after effective lipid lowering therapy with bezafibrate in a patient with Lipoatrophic Diabetes Mellitus a putative role for randle s cycle in its pathogenesis
Clinical Endocrinology, 1997Co-Authors: V. R. Panz, J. R. Wing, Frederick J. Raal, Mary-anne Kedda, Barry I. JoffeAbstract:This report describes a patient with Lipoatrophic Diabetes Mellitus (LDM), which is a rare clinical syndrome characterized by lipoatrophy and severe insulin resistance. Although a genetic abnormality is suspected in the development of LDM, no functional mutations in key domains of the insulin receptor gene were detected. Therapy was directed primarily at decreasing the availability of non-esterified fatty acids (NEFA), and thereby improving glucose tolerance (Randle's cycle), by the administration of a lipid-lowering drug, bezafibrate. Serial changes in fasting levels of the hormones of glucose homeostasis and lipids were measured, as well as glucose and insulin responses to a 75-g oral glucose challenge at onset and following 3 and 6 months of fibrate therapy. Progressive reductions in the patient's levels of triglycerides and NEFA were paralleled by an improvement in beta-cell function, a decrease in insulin resistance, and the attainment of normal glucose homeostasis. We conclude that the pathogenesis of LDM may be related primarily to abnormal regulation of lipid, rather than glucose, metabolism.
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Improved glucose tolerance after effective lipid‐lowering therapy with bezafibrate in a patient with Lipoatrophic Diabetes Mellitus: a putative role for Randle’s cycle in its pathogenesis?
Clinical endocrinology, 1997Co-Authors: V. R. Panz, J. R. Wing, Frederick J. Raal, Mary-anne Kedda, Barry I. JoffeAbstract:This report describes a patient with Lipoatrophic Diabetes Mellitus (LDM), which is a rare clinical syndrome characterized by lipoatrophy and severe insulin resistance. Although a genetic abnormality is suspected in the development of LDM, no functional mutations in key domains of the insulin receptor gene were detected. Therapy was directed primarily at decreasing the availability of non-esterified fatty acids (NEFA), and thereby improving glucose tolerance (Randle's cycle), by the administration of a lipid-lowering drug, bezafibrate. Serial changes in fasting levels of the hormones of glucose homeostasis and lipids were measured, as well as glucose and insulin responses to a 75-g oral glucose challenge at onset and following 3 and 6 months of fibrate therapy. Progressive reductions in the patient's levels of triglycerides and NEFA were paralleled by an improvement in beta-cell function, a decrease in insulin resistance, and the attainment of normal glucose homeostasis. We conclude that the pathogenesis of LDM may be related primarily to abnormal regulation of lipid, rather than glucose, metabolism.
J. R. Wing - One of the best experts on this subject based on the ideXlab platform.
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improved glucose tolerance after effective lipid lowering therapy with bezafibrate in a patient with Lipoatrophic Diabetes Mellitus a putative role for randle s cycle in its pathogenesis
Clinical Endocrinology, 1997Co-Authors: V. R. Panz, J. R. Wing, Frederick J. Raal, Mary-anne Kedda, Barry I. JoffeAbstract:This report describes a patient with Lipoatrophic Diabetes Mellitus (LDM), which is a rare clinical syndrome characterized by lipoatrophy and severe insulin resistance. Although a genetic abnormality is suspected in the development of LDM, no functional mutations in key domains of the insulin receptor gene were detected. Therapy was directed primarily at decreasing the availability of non-esterified fatty acids (NEFA), and thereby improving glucose tolerance (Randle's cycle), by the administration of a lipid-lowering drug, bezafibrate. Serial changes in fasting levels of the hormones of glucose homeostasis and lipids were measured, as well as glucose and insulin responses to a 75-g oral glucose challenge at onset and following 3 and 6 months of fibrate therapy. Progressive reductions in the patient's levels of triglycerides and NEFA were paralleled by an improvement in beta-cell function, a decrease in insulin resistance, and the attainment of normal glucose homeostasis. We conclude that the pathogenesis of LDM may be related primarily to abnormal regulation of lipid, rather than glucose, metabolism.
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Improved glucose tolerance after effective lipid‐lowering therapy with bezafibrate in a patient with Lipoatrophic Diabetes Mellitus: a putative role for Randle’s cycle in its pathogenesis?
Clinical endocrinology, 1997Co-Authors: V. R. Panz, J. R. Wing, Frederick J. Raal, Mary-anne Kedda, Barry I. JoffeAbstract:This report describes a patient with Lipoatrophic Diabetes Mellitus (LDM), which is a rare clinical syndrome characterized by lipoatrophy and severe insulin resistance. Although a genetic abnormality is suspected in the development of LDM, no functional mutations in key domains of the insulin receptor gene were detected. Therapy was directed primarily at decreasing the availability of non-esterified fatty acids (NEFA), and thereby improving glucose tolerance (Randle's cycle), by the administration of a lipid-lowering drug, bezafibrate. Serial changes in fasting levels of the hormones of glucose homeostasis and lipids were measured, as well as glucose and insulin responses to a 75-g oral glucose challenge at onset and following 3 and 6 months of fibrate therapy. Progressive reductions in the patient's levels of triglycerides and NEFA were paralleled by an improvement in beta-cell function, a decrease in insulin resistance, and the attainment of normal glucose homeostasis. We conclude that the pathogenesis of LDM may be related primarily to abnormal regulation of lipid, rather than glucose, metabolism.