Diurnal Variation in Response to Intravenous Glucose

Whichelow, Margaret J.; Sturge, R. A.; Keen, H.; Jarrett, R. J.; Stimmler, L.; Grainger, Susan

doi:10.1136/bmj.1.5906.488

Cited by 69 publications

(44 citation statements)

References 15 publications

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“…These observations are consistent with previous reports of a progressive impairment of insulin responses to oral glucose loads during the day [10][11][12][13][14]41]. Furthermore, insulin responses to intravenous glucose have been reported to be greater in the morning than in the evening [12,42]. The similarity in diurnal responses of plasma insulin between intravenous and oral glucose challenges obviates the participation of the enteroinsular axis in this phenomenon.…”

Section: Discussionsupporting

confidence: 82%

Effects of size, time of day and sequence of meal ingestion on carbohydrate tolerance in normal subjects

et al. 1983

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Summary. The effects of size, time of day and sequence of meal ingestion were determined in healthy subjects using a Latin square design. Plasma glucose, insulin and gastric inhibitory polypeptide, but not glucagon, were correlated with meal size. Plasma glucose, but not insulin, gastric inhibitory polypeptide or glucagon, were greater later in the day. The progressive decline in carbohydrate tolerance from 08.00 to 18.00h was associated with impaired insulin secretion estimated by C-peptide, and with impaired insulin action.

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Section: Discussionsupporting

confidence: 82%

Effects of size, time of day and sequence of meal ingestion on carbohydrate tolerance in normal subjects

et al. 1983

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“…In addition, glucose tolerance has been reported to be lower and insulin response slower when glucose is given orally either in the afternoon or evening than when it is given in the morning [18]. Similar diurnal insulin sensitivity has been reported in response to an intravenous glucose load [19]. The relatively impaired glucose tolerance observed in the afternoon or the evening is associated with a delayed insulin response to the glucose load, which is probably due to decreased sensitivity of pancreatic β cells to glucose [20].…”

Section: Diurnal Insulin Sensitivity In Normal Subjects and Patients supporting

confidence: 52%

Effects of Growth Hormone on Diurnal Insulin Sensitivity in Normal and Type 2 Diabetic Patients and Animal Models

Shih¹,

Ho²

2016

J Diabetes Metab

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This review addresses the effects of growth hormone on diurnal insulin sensitivity in normal, patients with type 2 diabetes mellitus (T2DM) and animal models described in our previous studies. Results confirmed the presence of diurnal insulin sensitivity, or greater insulin sensitivity in the morning, in normal subjects. The exact cause of this circadian rhythm in plasma glucose levels in healthy subjects has not been established, and nocturnal surges in growth hormone secretion remain a possible explanation. Results showed that growth hormone is an important factor controlling the diurnal variation of glucose tolerance and insulin sensitivity in rats. Data from our previous study provided direct evidence that the role of growth hormone in regulating insulin sensitivity in healthy subjects may be related to changes in the metabolic clearance rate of insulin and the metabolism of non-esterified fatty acids. A different circadian rhythm for plasma glucose appears to be present in patients with T2DM with nadirs in the early evening and peaks in the early morning, indicating greater insulin sensitivity in the evening. As in normal subjects, the exact cause of these circadian rhythms in the plasma glucose levels of patients with T2DM provided direct evidence that the reduction in insulin sensitivity may be due to the nocturnal surge of growth hormone in the early morning hours.

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“…Based on the analyses of both AIR and glucose tolerance, we strongly believe, however, that the decrease in postprandial insulin sensitivity is not due to diurnal variations in insulin sensitivity. In most studies, it has been observed that glucose tolerance is decreased in the afternoon or evening compared with the morning [37][38][39]; decreased glucose tolerance, in these studies, was shown to result from decreased insulin secretion [38][39][40], decreased insulin sensitivity [41,42] or both [37,43]. Although we observed decreased insulin sensitivity at 13.00 h, there is a noticeable difference to the above-mentioned reports on diurnal variation in glucose tolerance/insulin sensitivity; in our study, decreased insulin sensitivity is compensated by enhanced insulin secretion resulting in an even improved postprandial glucose tolerance when compared with respective postabsorptive values analysed in the morning.…”

Section: Discussionmentioning

confidence: 99%

Postprandial lipaemia induces an acute decrease of insulin sensitivity in healthy men independently of plasma NEFA levels

et al. 2006

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Aims/hypothesis: Typical Western diets cause postprandial lipaemia for 18 h per day. We tested the hypothesis that postprandial lipaemia decreases insulin sensitivity. Subjects, materials and methods: Employing a randomised crossover design, we administered two types of virtually isocaloric meals to ten healthy volunteers on two separate occasions. The meals (Meals 1 and 2) were both designed to produce a rise in triglycerides, but only Meal 1 generated a rise in NEFA, too. Insulin sensitivity, as quantified by an IVGTT with minimal model analysis, was calculated postabsorptively at 08.00 h and postprandially at 13.00 h, i.e. 3 h after meal ingestion. Results: Triglycerides rose from 0.91±0.31 mmol/l postabsorptively to 2.08±0.70 mmol/l postprandially with Meal 1 (p=0.005) and from 0.92±0.41 to 1.71±0.79 mmol/ l with Meal 2 (p=0.005). Neither the triglyceride levels at 13.00 h, nor the post-meal AUCs for triglycerides were statistically different between Meal 1 and Meal 2. NEFA rose from 0.44±0.17 mmol/l postabsorptively to 0.69±0.16 mmol/ l postprandially with Meal 1 (p=0.005) and showed no significant change with Meal 2 (0.46±0.31 mmol/l postabsorptively vs 0.36±0.32 mmol/l postprandially, p=0.09). Both the NEFA level at 13.00 h and the post-meal AUC for NEFA were significantly higher after Meal 1 than Meal 2. Compared with the postabsorptive state, insulin sensitivity decreased postprandially after each of the two meals to a comparable degree (Meal 1: −53%, p=0.02; Meal 2: −45%, p=0.005). Conclusions/interpretation: Our study reveals a drop in insulin sensitivity during postprandial lipaemia and strongly suggests that decreased insulin sensitivity is brought about by elevated plasma levels of triglyceride-rich lipoproteins independently of plasma NEFA levels.

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Diurnal Variation in Response to Intravenous Glucose

Cited by 69 publications

References 15 publications

Effects of size, time of day and sequence of meal ingestion on carbohydrate tolerance in normal subjects

Effects of size, time of day and sequence of meal ingestion on carbohydrate tolerance in normal subjects

Effects of Growth Hormone on Diurnal Insulin Sensitivity in Normal and Type 2 Diabetic Patients and Animal Models

Postprandial lipaemia induces an acute decrease of insulin sensitivity in healthy men independently of plasma NEFA levels

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