Tags

Type your tag names separated by a space and hit enter

Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans.
Diabetes Care. 2006 Aug; 29(8):1909-14.DC

Abstract

OBJECTIVE

To compare the pathophysiology of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in a more comprehensive and standardized fashion than has hitherto been done.

RESEARCH DESIGN AND METHODS

We studied 21 individuals with isolated IFG (IFG/normal glucose tolerance [NGT]), 61 individuals with isolated IGT (normal fasting glucose [NFG]/IGT), and 240 healthy control subjects (NFG/NGT) by hyperglycemic clamps to determine first- and second-phase insulin release and insulin sensitivity. Homeostasis model assessment (HOMA) indexes of beta-cell function (HOMA-%B) and insulin resistance (HOMA-IR) were calculated from fasting plasma insulin and glucose concentrations.

RESULTS

Compared with NFG/NGT, IFG/NGT had similar fasting insulin concentrations despite hyperglycemia; therefore, HOMA-IR was increased approximately 30% (P < 0.05), but clamp-determined insulin sensitivity was normal (P > 0.8). HOMA-%B and first-phase insulin responses were reduced approximately 35% (P < 0.002) and approximately 30% (P < 0.02), respectively, but second-phase insulin responses were normal (P > 0.5). NFG/IGT had normal HOMA-IR but approximately 15% decreased clamp-determined insulin sensitivity (P < 0.03). Furthermore, HOMA-%B was normal but both first-phase (P < 0.0003) and second-phase (P < 0.0001) insulin responses were reduced approximately 30%. IFG/NGT differed from NFG/IGT by having approximately 40% lower HOMA-%B (P < 0.012) and approximately 50% greater second-phase insulin responses (P < 0.005).

CONCLUSIONS

Since first-phase insulin responses were similarly reduced in IFG/NGT and NFG/IGT, we conclude that IFG is due to impaired basal insulin secretion and preferential resistance of glucose production to suppression by insulin, as reflected by fasting hyperglycemia despite normal plasma insulin concentrations and increased HOMA-IR, whereas IGT mainly results from reduced second-phase insulin release and peripheral insulin resistance, as reflected by reduced clamp-determined insulin sensitivity.

Authors+Show Affiliations

Department of Endocrinology, Carl T. Hayden VA Medical Center, Phoenix, AZ 85012, USA. christian.meyer@med.a.govNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16873801

Citation

Meyer, Christian, et al. "Different Mechanisms for Impaired Fasting Glucose and Impaired Postprandial Glucose Tolerance in Humans." Diabetes Care, vol. 29, no. 8, 2006, pp. 1909-14.
Meyer C, Pimenta W, Woerle HJ, et al. Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans. Diabetes Care. 2006;29(8):1909-14.
Meyer, C., Pimenta, W., Woerle, H. J., Van Haeften, T., Szoke, E., Mitrakou, A., & Gerich, J. (2006). Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans. Diabetes Care, 29(8), 1909-14.
Meyer C, et al. Different Mechanisms for Impaired Fasting Glucose and Impaired Postprandial Glucose Tolerance in Humans. Diabetes Care. 2006;29(8):1909-14. PubMed PMID: 16873801.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans. AU - Meyer,Christian, AU - Pimenta,Walkyria, AU - Woerle,Hans J, AU - Van Haeften,Timon, AU - Szoke,Ervin, AU - Mitrakou,Asimina, AU - Gerich,John, PY - 2006/7/29/pubmed PY - 2006/12/9/medline PY - 2006/7/29/entrez SP - 1909 EP - 14 JF - Diabetes care JO - Diabetes Care VL - 29 IS - 8 N2 - OBJECTIVE: To compare the pathophysiology of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in a more comprehensive and standardized fashion than has hitherto been done. RESEARCH DESIGN AND METHODS: We studied 21 individuals with isolated IFG (IFG/normal glucose tolerance [NGT]), 61 individuals with isolated IGT (normal fasting glucose [NFG]/IGT), and 240 healthy control subjects (NFG/NGT) by hyperglycemic clamps to determine first- and second-phase insulin release and insulin sensitivity. Homeostasis model assessment (HOMA) indexes of beta-cell function (HOMA-%B) and insulin resistance (HOMA-IR) were calculated from fasting plasma insulin and glucose concentrations. RESULTS: Compared with NFG/NGT, IFG/NGT had similar fasting insulin concentrations despite hyperglycemia; therefore, HOMA-IR was increased approximately 30% (P < 0.05), but clamp-determined insulin sensitivity was normal (P > 0.8). HOMA-%B and first-phase insulin responses were reduced approximately 35% (P < 0.002) and approximately 30% (P < 0.02), respectively, but second-phase insulin responses were normal (P > 0.5). NFG/IGT had normal HOMA-IR but approximately 15% decreased clamp-determined insulin sensitivity (P < 0.03). Furthermore, HOMA-%B was normal but both first-phase (P < 0.0003) and second-phase (P < 0.0001) insulin responses were reduced approximately 30%. IFG/NGT differed from NFG/IGT by having approximately 40% lower HOMA-%B (P < 0.012) and approximately 50% greater second-phase insulin responses (P < 0.005). CONCLUSIONS: Since first-phase insulin responses were similarly reduced in IFG/NGT and NFG/IGT, we conclude that IFG is due to impaired basal insulin secretion and preferential resistance of glucose production to suppression by insulin, as reflected by fasting hyperglycemia despite normal plasma insulin concentrations and increased HOMA-IR, whereas IGT mainly results from reduced second-phase insulin release and peripheral insulin resistance, as reflected by reduced clamp-determined insulin sensitivity. SN - 0149-5992 UR - https://www.unboundmedicine.com/medline/citation/16873801/Different_mechanisms_for_impaired_fasting_glucose_and_impaired_postprandial_glucose_tolerance_in_humans_ L2 - http://care.diabetesjournals.org/cgi/pmidlookup?view=long&amp;pmid=16873801 DB - PRIME DP - Unbound Medicine ER -