| 1. |
- Axelsen, Mette, 1965, et al.
(författare)
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Bedtime uncooked cornstarch supplement prevents nocturnal hypoglycaemia in intensively treated type 1 diabetes subjects.
- 1999
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Ingår i: Journal of internal medicine. - 0954-6820. ; 245:3, s. 229-36
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: The present study tests two interrelated hypotheses: (1) that bedtime ingestion of uncooked cornstarch exerts a lower and delayed nocturnal blood glucose peak compared with a conventional snack; (2) that bedtime carbohydrate supplement, administered as uncooked cornstarch, prevents nocturnal hypoglycaemia without altering metabolic control in intensively treated type 1 diabetes (IDDM) patients. DESIGN AND SUBJECTS: The above hypotheses were tested separately (1) by pooling and analysing data from two overnight studies of comparable groups of patients with non-insulin dependent diabetes mellitus (NIDDM) (14 and 10 patients, respectively), and (2) by a double-blind, randomized 4-week cross-over study in 12 intensively treated IDDM patients. SETTING: Sahlgrenska University Hospital, Göteborg. Sweden. INTERVENTIONS: (1) Ingestion of uncooked cornstarch and wholemeal bread (0.6 g of carbohydrates kg-1 body weight) and carbohydrate-free placebo at 22.00 h. (2) Intake of uncooked cornstarch (0.3 g kg-1 body weight) and carbohydrate-free placebo at 23.00 h. MAIN OUTCOME MEASURES: (1) Nocturnal glucose and insulin levels; (2) frequency of self-estimated hypoglycaemia (blood glucose [BG] levels < 3.0 mmol L-1) at 03.00 h, HbA1c and fasting lipids. RESULTS: Bedtime uncooked cornstarch ingestion led to a lower (2.9 +/- 0.5 vs. 5.2 +/- 0.6 mM, P = 0.01) and delayed (4.3 +/- 0.6 vs. 2.0 +/- 0.0 h, P < 0.01) BG peak, compared with a conventional snack, in NIDDM patients. Four weeks of bedtime uncooked cornstarch supplement, as compared with placebo, led to a 70% reduction in the frequency of self-estimated hypoglycaemia at 03.00 h (P < 0.05), without affecting HbA1c or fasting lipids in IDDM patients. CONCLUSIONS: Uncooked cornstarch, ingested at bedtime, mimicked the nocturnal glucose utilization profile following insulin replacement, with a peak in blood glucose after 4 h. In IDDM patients, bedtime uncooked cornstarch supplement diminished the number of self-estimated hypoglycaemic episodes, without adversely affecting HbA1c and lipid levels. Hence, bedtime uncooked cornstarch ingestion may be feasible to prevent a mid-nocturnal glycaemic decline following insulin replacement in IDDM and, based on the nocturnal blood glucose profile, may also be preferable compared with conventional snacks.
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| 2. |
- Carvalho, Eugénia, 1967, et al.
(författare)
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Impaired phosphorylation and insulin-stimulated translocation to the plasma membrane of protein kinase B/Akt in adipocytes from Type II diabetic subjects
- 2000
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Ingår i: Diabetologia. - 0012-186X. ; 43:9, s. 1107-15
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Tidskriftsartikel (refereegranskat)abstract
- AIMS/HYPOTHESIS: To examine protein kinase B/Akt distribution and phosphorylation in response to insulin in different subcellular fractions of human fat cells from healthy subjects and subjects with Type II (non-insulin-dependent) diabetes mellitus. METHODS: We prepared subcellular fractions of plasma membranes (PM), low density microsomes and cytosol and examined gene and protein expression as well as serine and threonine phosphorylation in response to insulin. RESULTS: Protein kinase B/Akt mRNA as well as total protein kinase B/Akt protein in whole-cell lysate and cytosol were similar in both groups. Insulin increased protein kinase B/Akt translocation to the the plasma membrane about twofold [(p < 0.03) in non-diabetic cells but this effect was impaired in diabetic cells (approximately 30%; p > 0.1)]. In both groups, protein kinase B/Akt threonine phosphorylation considerably increased in low density microsomes and cytosol whereas serine phosphorylation was predominant in the plasma membrane. Phosphatidylinositol-dependent kinase 1, which partially activates and phosphorylates protein kinase B/Akt on the specific threonine site, was predominant in cytosol but it was also recovered in low density microsomes. Serine phosphorylation in response to insulin was considerably reduced (50-70 %; p < 0.05) in diabetic cells but threonine phosphorylation was less reduced (approximately 20%). Wortmannin inhibited these effects of insulin supporting a role for PI3-kinase activation. CONCLUSION/INTERPRETATION: Insulin stimulates a differential subcellular pattern of phosphorylation of protein kinase B/Akt. Furthermore, insulin-stimulated translocation of protein kinase B/Akt to the plasma membrane, where serine phosphorylation and full activation occurs, is impaired in Type II diabetes. Threonine phosphorylation was much less reduced. This discrepancy may be related to differential activation of phosphatidylinositol 3-kinase in the different subcellular compartments and phosphatidylinositol-dependent kinase 1 having high affinity for phosphatidylinositol phosphate 3.
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| 3. |
- Norrsell, Ulf, 1937, et al.
(författare)
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Tactile directional sensibility and diabetic neuropathy.
- 2001
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Ingår i: Muscle & nerve. - 0148-639X. ; 24:11, s. 1496-502
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Tidskriftsartikel (refereegranskat)abstract
- Five different procedures used to diagnose neuropathy were compared in a "blind" study with diabetic patients. The aim was to evaluate tests of tactile directional sensibility. Three matched groups were examined, two groups with type I diabetes, either with or without suspected neuropathy, and one of healthy controls. Testing consisted of: (1) examination by a specialist in neurology, (2) electrophysiologic measurement of nerve conduction velocity and determination of cool sensitivity, and (3) determination of directional sensibility in two stages, with categorical and quantitative techniques. Abnormal test results were obtained for both groups of diabetic patients. Quantitatively measured directional sensibility had the highest sensitivity (89%) and specificity (85%) when calculated for patients who had received a diagnosis of neuropathy from the neurologist, despite one case of abnormal directional sensibility among the healthy controls. Conduction velocity testing was almost comparably sensitive (80%) and cool sensitivity, comparably specific (85%) when calculated in the same manner.
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| 4. |
- Smith, Ulf, 1943, et al.
(författare)
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Insulin signaling and action in fat cells: associations with insulin resistance and type 2 diabetes.
- 1999
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Ingår i: Annals of the New York Academy of Sciences. - 0077-8923. ; 892, s. 119-26
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Forskningsöversikt (refereegranskat)abstract
- Adipose tissue only accounts for a relatively small proportion (< 10%) of the peripheral glucose utilization in response to insulin. However, the fat cells may still play an important role in insulin resistance and Syndrome X through, for instance, its endocrine functions (production of leptin, TNF alpha, PAI-1, etc.) and involvement in lipid metabolism (FFA release and hydrolysis of triglycerides). The fat cells are also highly sensitive to insulin and may thus be used to elucidate molecular mechanisms for insulin resistance in man. Examinations of the intracellular signaling mechanisms for insulin in fat cells from individuals with Type 2 diabetes revealed markedly lower insulin-stimulated PI3-kinase activity. This was due to a pronounced reduction in the cellular expression of the docking protein, IRS 1, whereas expression of IRS 2 was normal. However, IRS 2-associated PI3-kinase activity was only approximately one-third of that found to be associated with IRS 1 in normal cells. Downstream activation and serine phosphorylation of PKB/Akt by insulin were also markedly reduced in Type 2 diabetes. Furthermore, the dose-response curve for this effect of insulin was similar to that for glucose transport in both normal and Type 2 diabetic cells. Thus, these data show that both PI3-kinase and PKB activation by insulin are markedly reduced in Type 2 diabetes. We also examined whether an attenuated activation of PI3-kinase by insulin can be seen in non-diabetic insulin-resistant states. Approximately 30% of healthy subjects with at least two first-degree relatives with Type 2 diabetes exhibited perturbations in IRS-1 expression and signaling. These individuals were characterized by insulin resistance as well as other markers of Syndrome X. Thus, impaired IRS-1 expression and downstream signaling events in fat cells in response to insulin are associated with insulin resistance and Syndrome X.
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| 5. |
- Smith, Ulf, 1943, et al.
(författare)
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Pathogenesis and treatment of diabetic vascular disease - illustrated by two cases
- 2006
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Ingår i: J Intern Med. - : Wiley. - 0954-6820. ; 260:5, s. 409-20
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Tidskriftsartikel (refereegranskat)abstract
- This publication is a summary of the presentations given at the First JIM Grand Round held at the Sahlgrenska University Hospital on 15 March 2006. The Grand Round was based on two case reports; a patient with type 2 diabetes and pronounced macrovascular disease and another patient with early microvascular disease combined with the macrovascular complications. The pathogenesis of the vascular complications and the current treatment regimens were discussed in relation to the history and examinations performed in these patients.
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