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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
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We are analyzing https://link.springer.com/article/10.1007/s00125-005-0092-4.

Title:
The effect of sensitisation to insulin with pioglitazone on fasting and postprandial lipid metabolism, lipoprotein modification by lipases, and lipid transfer activities in type 2 diabetic patients | Diabetologia
Description:
Aims/hypothesis Insulin resistance is thought to be central to the pathogenesis of diabetic dyslipidaemia. We hypothesised that improving insulin sensitivity would improve fasting and postprandial triglyceride metabolism in patients with type 2 diabetes. To this aim we studied fasting and postprandial lipaemia in type 2 diabetic patients before and after sensitisation to insulin with pioglitazone, compared with that observed in patients on an insulin-providing regime. Methods In a double-blind placebo-controlled protocol, 22 patients with type 2 diabetes were randomly allocated to receive either pioglitazone (45 mg/day) or glibenclamide (5 mg/day), for a 20-week period. Fasting and postprandial lipid metabolism were investigated at baseline and at the end of the treatment period. A group of non-diabetic subjects was also studied. Results Compared with glibenclamide treatment, pioglitazone treatment decreased fasting triglyceride, glucose and insulin levels and the homeostasis model assessment score of insulin resistance. Decreased fasting triglyceride after pioglitazone treatment was due to reduced VLDL triglyceride, particularly VLDL-2. Lipoprotein lipase activity was unchanged by pioglitazone treatment but hepatic lipase showed a significant decrease. Pioglitazone treatment lowered total postprandial triglyceride, as well as chylomicron- and chylomicron-remnant retinyl palmitate levels to normal. Glucose disposal improved but remained abnormal. Conclusions/interpretation Insulin sensitisation with pioglitazone has major effects in restoring postprandial lipaemia to normal, while also correcting fasting hypertriglyceridaemia; both factors may have consequences for atherogenic risk in diabetes.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Science
  • Education

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,016 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We can't see how the site brings in money.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

pioglitazone, treatment, patients, insulin, postprandial, triglyceride, article, google, scholar, plasma, diabetic, pubmed, cas, glibenclamide, fasting, control, subjects, type, diabetes, activity, metabolism, lipoprotein, vldl, hepatic, lipid, transfer, levels, disposal, lipase, controls, significant, chylomicron, resistance, baseline, effect, glucose, study, group, lipoproteins, nefa, activities, effects, lpl, protein, significantly, cholesterol, ldl, meal, table, reduction,

Topics {✒️}

double-blind placebo-controlled protocol peroxisome proliferator-activated receptor peroxisome proliferator-activated receptors lipoprotein particle size lipid transfer proteins [3h]tri-oleoyl glycerol [24] phosphoinositide 3-kinase-mediated event short-term acipimox decreases apob-lipoprotein-depleted plasma transfer proteins brought paired t-test analysis remove triglyceride-rich lipoproteins glucose–fatty acid cycle apolipoprotein c-iii levels rapid semi-micro method triglyceride-rich remnant particles receiving lipid-lowering therapy post-heparin plasma prepared phospholipid transfer protein triglyceride-rich lipoprotein remnants cholesteryl ester content paired t-test analyses fatty acid metabolism adipose-derived protein phospholipid transfer tended metabolic fuel selection privacy choices/manage cookies decreased fasting triglyceride postprandial lipid disposal insulin-dependent diabetic patients apolipoprotein c-iii postprandial lipid metabolism fructose-fed hamster lipid transfer activities high fat content van’t-laar apolipoproteins c-ii matching placebo tablets chylomicron remnant metabolism affect lipid metabolism homeostasis model assessment glibenclamide-treated patient group isocratic hplc chromatography md studentship award receive insulin-providing therapy increased triglyceride content human plasma lipoproteins de koning ejp saturated fat ratio=0 paired t-test

Questions {❓}

  • Jansen H, Verhoeven AJM, Sijbrands EJC (2002) Hepatic lipase: a pro- or anti-atherogenic protein?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:The effect of sensitisation to insulin with pioglitazone on fasting and postprandial lipid metabolism, lipoprotein modification by lipases, and lipid transfer activities in type 2 diabetic patients
         description:Insulin resistance is thought to be central to the pathogenesis of diabetic dyslipidaemia. We hypothesised that improving insulin sensitivity would improve fasting and postprandial triglyceride metabolism in patients with type 2 diabetes. To this aim we studied fasting and postprandial lipaemia in type 2 diabetic patients before and after sensitisation to insulin with pioglitazone, compared with that observed in patients on an insulin-providing regime. In a double-blind placebo-controlled protocol, 22 patients with type 2 diabetes were randomly allocated to receive either pioglitazone (45 mg/day) or glibenclamide (5 mg/day), for a 20-week period. Fasting and postprandial lipid metabolism were investigated at baseline and at the end of the treatment period. A group of non-diabetic subjects was also studied. Compared with glibenclamide treatment, pioglitazone treatment decreased fasting triglyceride, glucose and insulin levels and the homeostasis model assessment score of insulin resistance. Decreased fasting triglyceride after pioglitazone treatment was due to reduced VLDL triglyceride, particularly VLDL-2. Lipoprotein lipase activity was unchanged by pioglitazone treatment but hepatic lipase showed a significant decrease. Pioglitazone treatment lowered total postprandial triglyceride, as well as chylomicron- and chylomicron-remnant retinyl palmitate levels to normal. Glucose disposal improved but remained abnormal. Insulin sensitisation with pioglitazone has major effects in restoring postprandial lipaemia to normal, while also correcting fasting hypertriglyceridaemia; both factors may have consequences for atherogenic risk in diabetes.
         datePublished:2006-01-21T00:00:00Z
         dateModified:2006-01-21T00:00:00Z
         pageStart:527
         pageEnd:537
         sameAs:https://doi.org/10.1007/s00125-005-0092-4
         keywords:
            Chylomicron metabolism
            Glibenclamide
            Insulin resistance
            Lipase
            Lipid transfer proteins
            Lipoproteins
            Pioglitazone
            Postprandial lipid metabolism
            Thiazolidinedione
            Type 2 diabetes
            Internal Medicine
            Metabolic Diseases
            Human Physiology
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         isPartOf:
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               name:K. Al Majali
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                        name:UR 545 INSERM, Atherosclerosis Department, Pasteur Institute of Lille, and the Faculty of Pharmacy, Lille2 University, Lille, France
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               name:M-R. Taskinen
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                        name:Helsinki University Hospital, Helsinki, Finland
                        type:PostalAddress
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               name:D. J. Betteridge
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                     name:Royal Free and University College Medical School
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                        name:Department of Medicine, Royal Free and University College Medical School, London, UK
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ScholarlyArticle:
      headline:The effect of sensitisation to insulin with pioglitazone on fasting and postprandial lipid metabolism, lipoprotein modification by lipases, and lipid transfer activities in type 2 diabetic patients
      description:Insulin resistance is thought to be central to the pathogenesis of diabetic dyslipidaemia. We hypothesised that improving insulin sensitivity would improve fasting and postprandial triglyceride metabolism in patients with type 2 diabetes. To this aim we studied fasting and postprandial lipaemia in type 2 diabetic patients before and after sensitisation to insulin with pioglitazone, compared with that observed in patients on an insulin-providing regime. In a double-blind placebo-controlled protocol, 22 patients with type 2 diabetes were randomly allocated to receive either pioglitazone (45 mg/day) or glibenclamide (5 mg/day), for a 20-week period. Fasting and postprandial lipid metabolism were investigated at baseline and at the end of the treatment period. A group of non-diabetic subjects was also studied. Compared with glibenclamide treatment, pioglitazone treatment decreased fasting triglyceride, glucose and insulin levels and the homeostasis model assessment score of insulin resistance. Decreased fasting triglyceride after pioglitazone treatment was due to reduced VLDL triglyceride, particularly VLDL-2. Lipoprotein lipase activity was unchanged by pioglitazone treatment but hepatic lipase showed a significant decrease. Pioglitazone treatment lowered total postprandial triglyceride, as well as chylomicron- and chylomicron-remnant retinyl palmitate levels to normal. Glucose disposal improved but remained abnormal. Insulin sensitisation with pioglitazone has major effects in restoring postprandial lipaemia to normal, while also correcting fasting hypertriglyceridaemia; both factors may have consequences for atherogenic risk in diabetes.
      datePublished:2006-01-21T00:00:00Z
      dateModified:2006-01-21T00:00:00Z
      pageStart:527
      pageEnd:537
      sameAs:https://doi.org/10.1007/s00125-005-0092-4
      keywords:
         Chylomicron metabolism
         Glibenclamide
         Insulin resistance
         Lipase
         Lipid transfer proteins
         Lipoproteins
         Pioglitazone
         Postprandial lipid metabolism
         Thiazolidinedione
         Type 2 diabetes
         Internal Medicine
         Metabolic Diseases
         Human Physiology
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            type:ImageObject
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      author:
            name:K. Al Majali
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                  name:Royal Free and University College Medical School
                  address:
                     name:Department of Medicine, Royal Free and University College Medical School, London, UK
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                  type:Organization
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            name:M. B. Cooper
            affiliation:
                  name:Royal Free and University College Medical School
                  address:
                     name:Department of Medicine, Royal Free and University College Medical School, London, UK
                     type:PostalAddress
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                  address:
                     name:UR 545 INSERM, Atherosclerosis Department, Pasteur Institute of Lille, and the Faculty of Pharmacy, Lille2 University, Lille, France
                     type:PostalAddress
                  type:Organization
            type:Person
            name:G. Luc
            affiliation:
                  name:Lille2 University
                  address:
                     name:UR 545 INSERM, Atherosclerosis Department, Pasteur Institute of Lille, and the Faculty of Pharmacy, Lille2 University, Lille, France
                     type:PostalAddress
                  type:Organization
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                  name:Helsinki University Hospital
                  address:
                     name:Helsinki University Hospital, Helsinki, Finland
                     type:PostalAddress
                  type:Organization
            type:Person
            name:D. J. Betteridge
            affiliation:
                  name:Royal Free and University College Medical School
                  address:
                     name:Department of Medicine, Royal Free and University College Medical School, London, UK
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         name:Department of Medicine, Royal Free and University College Medical School, London, UK
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         name:UR 545 INSERM, Atherosclerosis Department, Pasteur Institute of Lille, and the Faculty of Pharmacy, Lille2 University, Lille, France
         type:PostalAddress
      name:Lille2 University
      address:
         name:UR 545 INSERM, Atherosclerosis Department, Pasteur Institute of Lille, and the Faculty of Pharmacy, Lille2 University, Lille, France
         type:PostalAddress
      name:Helsinki University Hospital
      address:
         name:Helsinki University Hospital, Helsinki, Finland
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            name:Royal Free and University College Medical School
            address:
               name:Department of Medicine, Royal Free and University College Medical School, London, UK
               type:PostalAddress
            type:Organization
      name:M. B. Cooper
      affiliation:
            name:Royal Free and University College Medical School
            address:
               name:Department of Medicine, Royal Free and University College Medical School, London, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:B. Staels
      affiliation:
            name:Lille2 University
            address:
               name:UR 545 INSERM, Atherosclerosis Department, Pasteur Institute of Lille, and the Faculty of Pharmacy, Lille2 University, Lille, France
               type:PostalAddress
            type:Organization
      name:G. Luc
      affiliation:
            name:Lille2 University
            address:
               name:UR 545 INSERM, Atherosclerosis Department, Pasteur Institute of Lille, and the Faculty of Pharmacy, Lille2 University, Lille, France
               type:PostalAddress
            type:Organization
      name:M-R. Taskinen
      affiliation:
            name:Helsinki University Hospital
            address:
               name:Helsinki University Hospital, Helsinki, Finland
               type:PostalAddress
            type:Organization
      name:D. J. Betteridge
      affiliation:
            name:Royal Free and University College Medical School
            address:
               name:Department of Medicine, Royal Free and University College Medical School, London, UK
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Medicine, Royal Free and University College Medical School, London, UK
      name:Department of Medicine, Royal Free and University College Medical School, London, UK
      name:UR 545 INSERM, Atherosclerosis Department, Pasteur Institute of Lille, and the Faculty of Pharmacy, Lille2 University, Lille, France
      name:UR 545 INSERM, Atherosclerosis Department, Pasteur Institute of Lille, and the Faculty of Pharmacy, Lille2 University, Lille, France
      name:Helsinki University Hospital, Helsinki, Finland
      name:Department of Medicine, Royal Free and University College Medical School, London, UK

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