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Article ; Online: Prediction of incident diabetes risk and structural equation modelling.

Radziuk, Jerry

The American journal of the medical sciences

2022 Volume 364, Issue 3, Page(s) 249–250

MeSH term(s)	Diabetes Mellitus/epidemiology ; Diabetes Mellitus, Type 2/epidemiology ; Humans ; Latent Class Analysis ; Risk Assessment ; Risk Factors
Language	English
Publishing date	2022-05-11
Publishing country	United States
Document type	Editorial
ZDB-ID	82078-7
ISSN	1538-2990 ; 0002-9629
ISSN (online)	1538-2990
ISSN	0002-9629
DOI	10.1016/j.amjms.2022.05.007
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Article ; Online: Sensitivity to insulin and its kinetics.

Radziuk, Jerry

Obesity (Silver Spring, Md.)

2017 Volume 25, Issue 2, Page(s) 282–283

Language	English
Publishing date	2017-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	2230457-5
ISSN	1930-739X ; 1071-7323 ; 1930-7381
ISSN (online)	1930-739X
ISSN	1071-7323 ; 1930-7381
DOI	10.1002/oby.21741
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Article ; Online: Homeostastic model assessment and insulin sensitivity/resistance.

Radziuk, Jerry

Diabetes

2014 Volume 63, Issue 6, Page(s) 1850–1854

MeSH term(s)	Animals ; Insulin Resistance/physiology ; Insulin-Secreting Cells/physiology ; Male
Language	English
Publishing date	2014-06
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db14-0116
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Article ; Online: The artificial pancreas.

Radziuk, Jerry

Diabetes

2012 Volume 61, Issue 9, Page(s) 2221–2224

MeSH term(s)	Blood Glucose/metabolism ; Diabetes Mellitus, Type 1/drug therapy ; Humans ; Insulin Infusion Systems ; Pancreas, Artificial
Chemical Substances	Blood Glucose
Language	English
Publishing date	2012-08-24
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db12-0647
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Article ; Conference proceedings: Glucose production in health and type 2 diabetes: measurement, regulation, and molecular basis. An overview.

Radziuk, Jerry

Journal of investigative medicine : the official publication of the American Federation for Clinical Research

2004 Volume 52, Issue 6, Page(s) 364–365

MeSH term(s)	Blood Glucose/analysis ; Blood Glucose/biosynthesis ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Humans
Chemical Substances	Blood Glucose
Language	English
Publishing date	2004-09
Publishing country	England
Document type	Congresses
ZDB-ID	1217870-6
ISSN	1708-8267 ; 1081-5589 ; 0009-9279
ISSN (online)	1708-8267
ISSN	1081-5589 ; 0009-9279
DOI	10.1136/jim-52-06-29
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Article: Insulin sensitivity and its measurement: structural commonalities among the methods.

Radziuk, J

The Journal of clinical endocrinology and metabolism

2000 Volume 85, Issue 12, Page(s) 4426–4433

Abstract: Insulin is the principal hormone of metabolic regulation. Reduced responses to insulin constitute an underlying feature of type 2 diabetes. It is, therefore, incumbent on those who work in this area (as well as many others) to characterize this response, ...

Abstract	Insulin is the principal hormone of metabolic regulation. Reduced responses to insulin constitute an underlying feature of type 2 diabetes. It is, therefore, incumbent on those who work in this area (as well as many others) to characterize this response, in as simple and consistent a way as possible, so that this measure can be used both in the investigational and clinical setting. This type of approach, although eminently useful, is necessarily an oversimplification. Not only does insulin sensitivity change in pathological situations, but also in normal physiology. Tissue-specific, metabolite-specific, as well as process-specific responses may be expected to occur. Variations also occur in time-depending on the physiological state of the individual (e.g. pregnancy, aging) or following diurnal rhythms. It is perhaps remarkable that any consistent assessment of overall insulin sensitivity can be made. The observation that this can often be achieved has led to hypotheses suggesting that sensitivity to insulin is primarily determined at a single site (tissue, metabolite). At the same time, there are many discussions about the inconsistencies inherent in different approaches to the measurement of this parameter, suggesting that some of these variants, metabolic or otherwise, could lead to the low correlation between methods sometimes seen. Nevertheless, most methods used in the assessment of insulin sensitivity examine the response to insulin of a single metabolite, glucose, primarily in the muscle and liver, and under fasting conditions and should, therefore, demonstrate insulin sensitivity that is comparable among methods.
MeSH term(s)	Animals ; Glucose Clamp Technique ; Glucose Tolerance Test ; Homeostasis ; Humans ; Insulin/pharmacology ; Insulin/physiology ; Insulin Resistance/physiology ; Liver/metabolism
Chemical Substances	Insulin
Language	English
Publishing date	2000-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/jcem.85.12.7025
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Article: Diurnal rhythm in endogenous glucose production is a major contributor to fasting hyperglycaemia in type 2 diabetes. Suprachiasmatic deficit or limit cycle behaviour?

Radziuk, J / Pye, S

Diabetologia

2006 Volume 49, Issue 7, Page(s) 1619–1628

Abstract: Aims/hypothesis: An increase in endogenous glucose production (EGP) is a major contributor to fasting morning hyperglycaemia in type 2 diabetes. This increase is dissipated with fasting, later in the day. To understand its origin, EGP, gluconeogenesis ... ...

Abstract	Aims/hypothesis: An increase in endogenous glucose production (EGP) is a major contributor to fasting morning hyperglycaemia in type 2 diabetes. This increase is dissipated with fasting, later in the day. To understand its origin, EGP, gluconeogenesis and hormones that regulate metabolism were measured over 24 h. We hypothesised that EGP, and therefore glycaemia, would demonstrate a centrally mediated circadian rhythm in type 2 diabetes. Subjects and methods: Seven subjects with type 2 diabetes and six age- and BMI-matched control subjects, fasting after breakfast (08.00 h), underwent a further 24-h fast, with the infusion of [U-(13)C]glucose and [3-(14)C]lactate, starting at 14.00 h. The MCR and production of total and gluconeogenic glucose were determined from the tracer concentrations using compartmental analysis. Results: MCR was near constant: 1.73+/-0.10 in control and 1.40+/-0.14 ml kg(-1) min(-1) in diabetic subjects (p=0.04). EGP in diabetes rose gradually overnight from 8.2+/-0.7 to 11.3+/-0.5 micromol kg(-1) min(-1) at 06.00 h (p<0.05). Glucose utilisation lagged EGP, rising from 8.5+/-0.6 to 10.5+/-0.4 micromol kg(-1) min(-1) (p<0.05), inducing a fall in glycaemia from a peak of 8.0+/-0.5 mmol/l to 6.3+/-0.4 mmol/l (p<0.05). Cortisol and melatonin showed diurnal variations, whereas insulin, glucagon and leptin did not. Melatonin was most closely related to EGP, but its secretion was attenuated in diabetes (p<0.05). Conclusions/interpretation: In type 2 diabetes, EGP and gluconeogenesis display diurnal rhythms that drive the fasting hyperglycaemia and are absent in healthy control subjects. The rise in EGP may be related to a deficit in suprachiasmatic nucleus activity in diabetes, or result from non-linear behaviour plus a transition from a normal steady state to a limit cycle pattern in diabetes, or both.
MeSH term(s)	Blood Glucose/analysis ; Circadian Rhythm ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/metabolism ; Fasting/blood ; Fasting/metabolism ; Female ; Glucagon/blood ; Glucose/biosynthesis ; Glucose/metabolism ; Homeostasis ; Humans ; Hyperglycemia/etiology ; Insulin/blood ; Male ; Middle Aged ; Nonlinear Dynamics ; Suprachiasmatic Nucleus/physiopathology
Chemical Substances	Blood Glucose ; Insulin ; Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2006-07
Publishing country	Germany
Document type	Controlled Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-006-0273-9
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Article: The liver and glycogen metabolism.

Radziuk, J

JPEN. Journal of parenteral and enteral nutrition

1991 Volume 15, Issue 3, Page(s) 77S–81S

Abstract: It was shown that the liver is not the major site of removal of glucose after a carbohydrate meal in man. Fractional extractions varied from 5 to 10%. Alternative substrates for postprandial hepatic glycogen synthesis were therefore sought. It was ... ...

Abstract	It was shown that the liver is not the major site of removal of glucose after a carbohydrate meal in man. Fractional extractions varied from 5 to 10%. Alternative substrates for postprandial hepatic glycogen synthesis were therefore sought. It was demonstrated than, in man, about 60% of hepatic glycogen was formed from gluconeogenetic substrates. Since significant excursions occur only in plasma lactate after glucose loading, this was deemed the most likely substrate under these circumstances. By differential sampling across the liver and the gut in a conscious pig model, it was found that the liver takes up enough lactate (fractional extraction of 40-50%) to account for the gluconeogenetic production of glycogen. Forty percent of this arises from the gut. Muscle (as represented by the forearm in man) does not contribute lactate during glucose loading, suggesting that other tissues such as the skin are of importance. The gluconeogenetic process may be an important site for the obligatory tissue production of lactate.
MeSH term(s)	Animals ; Gluconeogenesis ; Glucose/metabolism ; Glucose-6-Phosphate ; Glucosephosphates/metabolism ; Glycogen/biosynthesis ; Humans ; Lactates/metabolism ; Lactic Acid ; Liver/metabolism ; Models, Biological
Chemical Substances	Glucosephosphates ; Lactates ; Lactic Acid (33X04XA5AT) ; Glucose-6-Phosphate (56-73-5) ; Glycogen (9005-79-2) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	1991-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	800861-9
ISSN	0148-6071
ISSN	0148-6071
DOI	10.1177/014860719101500377S
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Article: Tracer studies of liver metabolism.

Radziuk, J

Hormone and metabolic research. Supplement series

1990 Volume 24, Page(s) 31–40

Abstract: We have attempted to show a number of uses of tracers both as enhancing the information obtained in arterio-venous difference studies and in allowing the collection of data on hepatic metabolism--glucose production, glycogen formation, etc. in a ... ...

Abstract	We have attempted to show a number of uses of tracers both as enhancing the information obtained in arterio-venous difference studies and in allowing the collection of data on hepatic metabolism--glucose production, glycogen formation, etc. in a noninvasive fashion. We have demonstrated, using these methods, that (1) The fractional extraction of glucose by the liver during glucose loading is about 5%; (2) This extraction can lead to significant hepatic glucose uptake (25 g after 100 g glucose load); (3) Only some of this glucose (10 g) is taken up directly into glycogen; (4) The remainder of the glycogen formed following a glucose load (15 g) is synthesized by gluconeogenetic pathways; (5) This gluconeogenesis takes place primarily from lactate which is taken up avidly by the liver--50-60% extracted; (6) This lactate arises from the gut (40%) and from the liver itself (at least 10%) with the remainder from other peripheral obligate lactate producing tissue; (7) It was also shown that the amount and pathways of hepatic glycogen production after oral and intravenous glucose loading is very similar and that the major effects on glucose tolerance take place in peripheral tissues such as the forearm.
MeSH term(s)	Animals ; Carbon Radioisotopes ; Glucose/metabolism ; Humans ; Kinetics ; Lactates/metabolism ; Liver/metabolism ; Liver Circulation ; Liver Glycogen/biosynthesis ; Models, Biological ; Radioisotope Dilution Technique ; Tritium
Chemical Substances	Carbon Radioisotopes ; Lactates ; Liver Glycogen ; Tritium (10028-17-8) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	1990
Publishing country	Germany
Document type	Journal Article ; Review
ISSN	0170-5903
ISSN	0170-5903
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Article: Hepatic glycogen in humans. I. Direct formation after oral and intravenous glucose or after a 24-h fast.

Radziuk, J

The American journal of physiology

1989 Volume 257, Issue 2 Pt 1, Page(s) E145–57

Abstract: The formation of hepatic glycogen by the direct pathway is assessed in humans 1) after a 12-h fast and oral loading (100 g) or 2) intravenous infusion (90 g) and 3) after a 24-h fast and the same oral glucose load. The methodology used is based on the ... ...

Abstract	The formation of hepatic glycogen by the direct pathway is assessed in humans 1) after a 12-h fast and oral loading (100 g) or 2) intravenous infusion (90 g) and 3) after a 24-h fast and the same oral glucose load. The methodology used is based on the double tracer method. [3-3H]glucose is infused at a constant rate for the determination of the metabolic clearance of glucose. [1-14C]glucose is administered with the glucose load. One hour after absorption or the intravenous glucose infusion is terminated, a glucagon infusion is initiated to mobilize the glycogen labeled with [1-14C]glucose and formed during the absorptive period. At this time a third tracer, [6-3H]glucose, is administered to measure glucose clearance. It was found that after the 12-h fast and oral glucose loading 7.2 +/- 1.1 g of hepatic glycogen appears to be formed directly from glucose compared with 8.4 +/- 1.0 g after the same load and a 24-h fast and 8.5 +/- 0.4 g after a 12-h fast and an equivalent intravenous glucose infusion. When the amount of label ([14C]glucose) mobilized that was not corrected for metabolic recycling was calculated, the data suggested that the amount of glycogen formed by gluconeogenic pathways was probably at least equal to that formed by direct uptake. It was also approximately 60% greater after a 24-h fast. It can be concluded that the amount of hepatic glycogen formed directly from glucose during glucose loading is not significantly altered by the route of entry or the extension of the fasting period to 24 h. The data suggest, however, that gluconeogenetic formation of glycogen increases with fasting.
MeSH term(s)	Adult ; Blood Glucose/metabolism ; Carbon Radioisotopes ; Dietary Carbohydrates/metabolism ; Fasting ; Female ; Glucagon/pharmacology ; Glucose/administration & dosage ; Glucose/metabolism ; Humans ; Infusions, Intravenous ; Kinetics ; Liver Glycogen/biosynthesis ; Male ; Mathematics ; Models, Theoretical ; Radioisotope Dilution Technique ; Time Factors ; Tritium
Chemical Substances	Blood Glucose ; Carbon Radioisotopes ; Dietary Carbohydrates ; Liver Glycogen ; Tritium (10028-17-8) ; Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	1989-08
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2948-8
ISSN	0002-9513
ISSN	0002-9513
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