Glucose Dynamics in Normal Subjects and Diabetic Patients before and after a Glucose Load

Forbath, N.; Hetenyi, G

doi:10.2337/diab.15.11.778

Cited by 59 publications

(33 citation statements)

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“…For example, Christensen and Orskov reported that human forearm glucose uptake and not simultaneously measured plasma glucose levels was highly correlated with the level of endogenously secreted insulin (21). Forbath and Hetenyi demonstrated that in the basal state glucose turnover was the same in normal and diabetic subjects even though the diabetic subjects had fasting hyperglycemia (22) and on the basis of the present study might be expected to have similar basal insulin levels. Thus, subjects with different plasma glucose levels and comparable basal insulin levels may still have the same rates of glucose turnover.…”

Section: Discussionmentioning

confidence: 75%

Acute and steady-state insulin responses to glucose in nonobese diabetic subjects

Lerner¹,

Porte²

1972

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 75%

Acute and steady-state insulin responses to glucose in nonobese diabetic subjects

Lerner¹,

Porte²

1972

J. Clin. Invest.

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“…Several publications have documented a correlation between fasting plasma glucose concentration (measured at -8 a.m.) and Ra (measured from 8 to 10 a.m.) (3,4,(7)(8)(9), and concluded that hepatic overproduction of glucose is primarily responsible for maintenance of the enlarged plasma glucose pool in patients with NIDDM (9, 10). The data in Fig.…”

Section: Discussionmentioning

confidence: 99%

“…R. has also been shown to be increased in such patients (3)(4)(5)(6)(7)(8)(9) and statistically significant correlations have been documented between measurement of Ra and fasting plasma glucose concentration (3,4,(7)(8)(9). Based upon such considerations, it has been suggested that fasting hyperglycemia in NIDDM is due to an increase in Ra, whereas the defect in Rd accounts for postprandial hyperglycemia (3,4,9,10). This generalization is primarily based upon studies performed in the morning, after an overnight fast, in which Ra is measured over an -2-h period, i.e., from 8 to 10 a.m., and the observed value is correlated with plasma glucose concentration at 8 a.m. We were concerned about the results of studies carried out in this manner for two reasons.…”

mentioning

confidence: 99%

“…On the other hand, after an overnight fast Rd can be greater than normal in patients with NIDDM with significant fasting hyperglycemia (1). R. has also been shown to be increased in such patients (3)(4)(5)(6)(7)(8)(9) and statistically significant correlations have been documented between measurement of Ra and fasting plasma glucose concentration (3,4,(7)(8)(9). Based upon such considerations, it has been suggested that fasting hyperglycemia in NIDDM is due to an increase in Ra, whereas the defect in Rd accounts for postprandial hyperglycemia (3,4,9,10).…”

mentioning

confidence: 99%

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Relationship between plasma glucose and insulin concentration, glucose production, and glucose disposal in normal subjects and patients with non-insulin-dependent diabetes.

Chen¹,

Jeng²,

Hollenbeck³

et al. 1988

J. Clin. Invest.

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The changes in hepatic glucose production (R.), tissue glucose disposal (Rd), and plasma glucose and insulin concentration that took place over a 16-h period from 10 to 2 p.m. were documented in 14 individuals; 8 with non-insulin-dependent diabetes mellitus (NIDDM) and 6 with normal glucose tolerance. Values for R. were higher than normal in patients with NIDDM at 10 p.m. (4.73±0.41 vs. 3.51±0.36 mg/kg per min P < 0.001), but fell at a much faster rate throughout the night than that seen in normal subjects. As a consequence, the difference between R. in normal individuals and patients with NIDDM progressively narrowed, and by 2 p.m, had ceased to exist (1.75±0.61 vs. 1.67±0.47 mg/kg per min, P = NS).Plasma glucose concentration also declined in patients with NIDDM over the same period of time, but they remained quite hyperglycemic, and the value of 245±27 mg/dl at 2 p.m. was about three times greater than in normal individuals. Plasma insulin concentrations also fell progressively from 10 to 2 p.m., and were similar in both groups throughout most of the 16-h study period. Thus, the progressive decline in R. in patients with NIDDM occurred despite concomitant falls in both plasma glucose and insulin concentration. Glucose disposal rates also fell progressively in both groups, but the magnitude of the fall was greater in patients with NIDDM. Consequently, Rd in patients with NIDDM was higher at 10 p.m. (3.97±0.48 vs. 3.25±0.13 mg/kg per min, P < 0.001) and lower the following day at 2 p.m. (1.64±0.21 vs. 1.97±0.35 mg/kg per min, P < 0.01). These results indicate that a greatly expanded pool size can exist in patients with NIDDM at a time when values for R. are identical to those in normal subjects studied under comparable conditions, which suggests that fasting hyperglycemia in NIDDM is not simply a function of an increase in R1. Introduction Hyperglycemia can only develop when the rate of entry of

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“…The endogenous glucose turnover rate in maturityonset diabetes in man is variously reported as decreased (1, 2), normal (3)(4)(5)(6)(7)(8)(9)(10) and increased (11,12).…”

Section: Introductionmentioning

confidence: 99%

Glucose Turnover and Disposal in Maturity-Onset Diabetes

Bowen¹,

Moorhouse²

1973

J. Clin. Invest.

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A B S T R A C T The glucose turnover rate in maturityonset diabetes in man has been variously reported as increased, normal, and decreased. The present experiments suggest that these discrepancies may have been due to methodology, and to nonrecognition of a circadian cycle in the glucose turnover rate that is present in health, and marked in diabetes.During the early morning hours the glucose turnover rate in maturity-onset diabetes is increased in proportion to the fasting blood glucose level. It may reach three to four times the rate found in health. During the evening hours the increments are about one-half as great.The glucose outflow rate constant, k, lower in diabetes than in health, is also lower in both groups in the evening than in the morning.An analysis of the relative contributions of glucose overproduction and underutilization to the development of hyperglycemia in maturity-onset diabetes indicates that overproduction is the greater factor. The relative role of underutilization appears to increase as the fasting blood glucose level increases.The circulating glucose oxidation rate in maturityonset diabetes is only slightly lower than in health, but the fraction oxidized is markedly lower, and only a small fraction is excreted.The principal conclusion is that in maturity-onset diabetes there is a hypertrophied flux of endogenous glucose, most of which is neither oxidized nor excreted. The precursors and the qualitative and quantitative metabolic fates of this excess glucose are unknown.

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Glucose Dynamics in Normal Subjects and Diabetic Patients before and after a Glucose Load

Cited by 59 publications

References 0 publications

Acute and steady-state insulin responses to glucose in nonobese diabetic subjects

Acute and steady-state insulin responses to glucose in nonobese diabetic subjects

Relationship between plasma glucose and insulin concentration, glucose production, and glucose disposal in normal subjects and patients with non-insulin-dependent diabetes.

Glucose Turnover and Disposal in Maturity-Onset Diabetes

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