J E Gerich

University of Rochester, Rochester, New York, United States

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Publications (357)2876.74 Total impact

  • Mazen Alsahli, John E. Gerich
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    ABSTRACT: Hypoglycemia is a major problem associated with substantial morbidity and mortality in patients with diabetes and is often a major barrier to achieving optimal glycemic control. Chronic kidney disease not only is an independent risk factor for hypoglycemia but also augments the risk of hypoglycemia that is already present in people with diabetes. This article summarizes our current knowledge of the epidemiology, pathogenesis, and morbidity of hypoglycemia in patients with diabetes and chronic kidney disease and reviews therapeutic considerations in this situation. PubMed and MEDLINE were searched for literature published in English from January 1989 to May 2014 for diabetes mellitus, hypoglycemia, chronic kidney disease, and chronic renal insufficiency.
    Mayo Clinic Proceedings. 10/2014;
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    ABSTRACT: Background The objective of this paper is to evaluate the pharmacokinetics (PK), efficacy and safety of lixisenatide (subcutaneous injection) in elderly (≥65 years) and very elderly (≥75 years) patients with type 2 diabetes mellitus (T2DM).Methods We conducted a Phase I, single-centre, open-label study to evaluate the safety and pharmacokinetics of a single lixisenatide 20 µg dose, and a pooled analysis of six randomized, placebo-controlled, Phase III studies (12- or 24-month duration) that evaluated glycaemic parameters and safety in patients receiving lixisenatide 20 µg once daily or placebo.ResultsThe PK study included 36 healthy subjects, including 18 elderly healthy subjects (≥65 years) and 18 matched young healthy subjects (18–45 years). The pooled analysis included 3188 patients, including 2565 patients <65 years and 623 patients ≥65 years (including 79 patients ≥75 years). Mean exposure with lixisenatide 20 µg was ~30% higher in elderly than in young subjects and the terminal half-life was prolonged by ~1.6 times. Cmax and tmax were comparable in both groups. Equal numbers of elderly and young subjects reported treatment-emergent adverse events (TEAEs), the majority of which were gastrointestinal disorders. In the pooled analysis, lixisenatide 20 µg once daily provided significant reductions in HbA1c versus placebo for all age groups. There was a similar incidence of TEAEs across all age groups (range: 69–73%). The incidence of symptomatic hypoglycaemia was generally comparable between lixisenatide- and placebo-treated patients.Conclusion These data suggest that lixisenatide is effective and well tolerated in elderly and very elderly patients with T2DM. This article is protected by copyright. All rights reserved.
    Diabetes/Metabolism Research and Reviews 08/2014; · 2.97 Impact Factor
  • Farhad M. Hasan, Mazen Alsahli, John E. Gerich
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    ABSTRACT: The kidney plays an important role in glucose homeostasis via its production, utilization, and, most importantly, reabsorption of glucose from glomerular filtrate which is largely mediated via the sodium glucose co-transporter 2 (SGLT2). Pharmacological inhibition of SGLT2 increases urinary glucose excretion and decreases plasma glucose levels in an insulin-independent manner. Agents that inhibit SGLT2 represent a novel class of drugs, which has recently become available for treatment of type 2 diabetes. This article summarizes the rationale for use of these agents and reviews available clinical data on their efficacy, safety, and risks/benefits.
    Diabetes research and clinical practice 01/2014; · 2.74 Impact Factor
  • Mazen Alsahli, John E Gerich
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    ABSTRACT: Hypoglycemia remains a common problem for patients with diabetes and is associated with substantial morbidity and mortality. This article summarizes our current knowledge of the epidemiology, pathogenesis, risk factors, and complications of hypoglycemia in patients with diabetes and discusses prevention and treatment strategies.
    Endocrinology and metabolism clinics of North America 12/2013; 42(4):657-76. · 3.56 Impact Factor
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    ABSTRACT: OBJECTIVE To compare efficacy and safety of lixisenatide once daily versus exenatide twice daily in type 2 diabetes inadequately controlled with metformin.RESEARCH DESIGN AND METHODS Adults with diabetes inadequately controlled (HbA1c 7-10%) with metformin were randomized to lixisenatide 20 μg once daily (n = 318) or exenatide 10 μg twice daily (n = 316) in a 24-week (main period), open-label, parallel-group, multicenter study. The primary objective was a noninferiority assessment of lixisenatide versus exenatide in HbA1c change from baseline to week 24.RESULTSLixisenatide once daily demonstrated noninferiority in HbA1c reduction versus exenatide twice daily. The LS mean change was -0.79% (mean decrease 7.97 to 7.17%) for lixisenatide versus -0.96% (mean ± SD 7.96 to 7.01%) for exenatide, and treatment difference was 0.17% (95% CI, 0.033-0.297), meeting a predefined noninferiority upper CI margin of 0.4%. Responder rate (HbA1c <7.0%) and improvements in fasting plasma glucose were comparable. Both agents induced weight loss (from 94.5 to 91.7 kg and from 96.7 to 92.9 kg with lixisenatide and exenatide, respectively). Incidence of adverse events (AEs) was similar for lixisenatide and exenatide, as was incidence of serious AEs (2.8 and 2.2%, respectively). Discontinuations attributable to AEs occurred in 33 lixisenatide (10.4%) and 41 exenatide (13.0%) patients. In the lixisenatide group, fewer participants experienced symptomatic hypoglycemia (2.5 vs. 7.9%; P < 0.05), with fewer gastrointestinal events (especially nausea; 24.5 vs. 35.1%; P < 0.05).CONCLUSIONS Add-on lixisenatide once daily in type 2 diabetes inadequately controlled with metformin demonstrated noninferior improvements in HbA1c, with slightly lower mean weight loss, lower incidence of hypoglycemia, and better gastrointestinal tolerability compared with exenatide twice daily.
    Diabetes care 05/2013; · 7.74 Impact Factor
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    John Gerich
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    ABSTRACT: Postprandial plasma glucose concentrations are an important contributor to glycemic control. There is evidence suggesting that postprandial hyperglycemia may be an independent risk factor for cardiovascular disease. Glucagon-like peptide-1 (GLP-1) receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors are antidiabetic agents that predominantly reduce postprandial plasma glucose levels. DPP-4 inhibitors are associated with fewer gastrointestinal side effects than GLP-1 receptor agonists and are administered orally, unlike GLP-1 analogs, which are administered as subcutaneous injections. GLP-1 receptor agonists are somewhat more effective than DPP-4 inhibitors in reducing postprandial plasma glucose and are usually associated with significant weight loss. For these reasons, GLP-1 receptor agonists are generally preferred over DPP-4 inhibitors as part of combination treatment regimens in patients with glycated hemoglobin levels above 8.0%. This article reviews the pathogenesis of postprandial hyperglycemia, the mechanisms by which GLP-1 receptor agonists and DPP-4 inhibitors reduce postprandial plasma glucose concentrations, and the results of recent clinical trials (ie, published 2008 to October 2012) that evaluated the effects of these agents on postprandial plasma glucose levels when evaluated as monotherapy compared with placebo or as add-on therapy to metformin, a sulfonylurea, or insulin. Findings from recent clinical studies suggest that both GLP-1 receptor agonists and DPP-4 inhibitors could become valuable treatment options for optimizing glycemic control in patients unable to achieve glycated hemoglobin goals on basal insulin, with the added benefits of weight loss and a low risk of hypoglycemia.
    International Journal of General Medicine 01/2013; 6:877-895.
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    ABSTRACT: To assess efficacy and safety of lixisenatide monotherapy in type 2 diabetes. Randomized, double-blind, 12-week study of 361 patients not on glucose-lowering therapy (HbA(1c) 7-10%) allocated to one of four once-daily subcutaneous dose increase regimens: lixisenatide 2-step (10 μg for 1 week, 15 μg for 1 week, and then 20 μg; n = 120), lixisenatide 1-step (10 μg for 2 weeks and then 20 μg; n = 119), placebo 2-step (n = 61), or placebo 1-step (n = 61) (placebo groups were combined for analyses). Primary end point was HbA(1c) change from baseline to week 12. Once-daily lixisenatide significantly improved HbA(1c) (mean baseline 8.0%) in both groups (least squares mean change vs. placebo: -0.54% for 2-step, -0.66% for 1-step; P < 0.0001). Significantly more lixisenatide patients achieved HbA(1c) <7.0% (52.2% 2-step, 46.5% 1-step) and ≤ 6.5% (31.9% 2-step, 25.4% 1-step) versus placebo (26.8% and 12.5%, respectively; P < 0.01). Lixisenatide led to marked significant improvements of 2-h postprandial glucose levels and blood glucose excursions measured during a standardized breakfast test. A significant decrease in fasting plasma glucose was observed in both lixisenatide groups versus placebo. Mean decreases in body weight (∼2 kg) were observed in all groups. The most common adverse events were gastrointestinal-nausea was the most frequent (lixisenatide 23% overall, placebo 4.1%). Symptomatic hypoglycemia occurred in 1.7% of lixisenatide and 1.6% of placebo patients, with no severe episodes. Safety/tolerability was similar for the two dose regimens. Once-daily lixisenatide monotherapy significantly improved glycemic control with a pronounced postprandial effect (75% reduction in glucose excursion) and was safe and well tolerated in type 2 diabetes.
    Diabetes care 03/2012; 35(6):1225-31. · 7.74 Impact Factor
  • John E Gerich, Arnaud Bastien
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    ABSTRACT: Dapagliflozin is a highly selective sodium-glucose co-transporter 2 inhibitor developed for the treatment of Type 2 diabetes mellitus. Its inhibition of sodium-glucose co-transporter 2 blocks glucose reabsorption in the proximal tubule of the kidney, increasing renal glucose excretion via the urine, resulting in reduction of glycated hemoglobin, fasting plasma glucose and postprandial plasma glucose in patients with Type 2 diabetes mellitus. The pharmacokinetics and pharmacodynamics of dapagliflozin are suitable for once-daily dosing. Dapagliflozin improves glycemic control when used as monotherapy and when used in combination with other antidiabetic treatments. Throughout all phases of clinical studies, dapagliflozin was generally well tolerated. Increased events suggestive of urinary tract and genital infections have been reported; most resolved with conventional treatment. Unexpected numerical imbalances between dapagliflozin and comparator were noted for breast and bladder cancers. The potential for increased cancer risk with dapagliflozin needs to be further assessed.
    Expert Review of Clinical Pharmacology 11/2011; 4(6):669-83.
  • John Gerich
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    ABSTRACT: Attenuation of the prandial incretin effect, mediated by glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), contributes to hyperglycemia in type 2 diabetes mellitus (T2DM). Since the launch of sitagliptin in 2006, a compelling body of evidence has accumulated showing that dipeptidyl peptidase-4 (DPP-4) inhibitors, which augment endogenous GLP-1 and GIP levels, represent an important advance in the management of T2DM. Currently, three DPP-4 inhibitors - sitagliptin, vildagliptin and saxagliptin - have been approved in various countries worldwide. Several other DPP-4 inhibitors, including linagliptin and alogliptin, are currently in clinical development. As understanding of, and experience with, the growing number of DPP-4 inhibitors broadens, increasing evidence suggests that the class may offer advantages over other antidiabetic drugs in particular patient populations. The expanding evidence base also suggests that certain differences between DPP-4 inhibitors may prove to be clinically significant. This therapeutic diversity should help clinicians tailor treatment to the individual patient, thereby increasing the proportion that safely attain target HbA(1c) levels, and reducing morbidity and mortality. This review offers an overview of DPP-4 inhibitors in T2DM and suggests some characteristics that may provide clinically relevant differentiators within this class.
    Diabetes research and clinical practice 11/2010; 90(2):131-40. · 2.74 Impact Factor
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    J E Gerich
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    ABSTRACT: Considerable data have accumulated over the past 20 years, indicating that the human kidney is involved in the regulation of glucose via gluconeogenesis, taking up glucose from the circulation, and by reabsorbing glucose from the glomerular filtrate. In light of the development of glucose-lowering drugs involving inhibition of renal glucose reabsorption, this review summarizes these data. Medline was searched from 1989 to present using the terms 'renal gluconeogenesis', 'renal glucose utilization', 'diabetes mellitus' and 'glucose transporters'. The human liver and kidneys release approximately equal amounts of glucose via gluconeogenesis in the post-absorptive state. In the postprandial state, although overall endogenous glucose release decreases substantially, renal gluconeogenesis increases by approximately twofold. Glucose utilization by the kidneys after an overnight fast accounts for approximately 10% of glucose utilized by the body. Following a meal, glucose utilization by the kidney increases. Normally each day, approximately 180 g of glucose is filtered by the kidneys; almost all of this is reabsorbed by means of sodium-glucose co-transporter 2 (SGLT2), expressed in the proximal tubules. However, the capacity of SGLT2 to reabsorb glucose from the renal tubules is finite and, when plasma glucose concentrations exceed a threshold, glucose appears in the urine. Handling of glucose by the kidney is altered in Type 2 diabetes mellitus (T2DM): renal gluconeogenesis and renal glucose uptake are increased in both the post-absorptive and postprandial states, and renal glucose reabsorption is increased. Specific SGLT2 inhibitors are being developed as a novel means of controlling hyperglycaemia in T2DM.
    Diabetic Medicine 02/2010; 27(2):136-42. · 3.24 Impact Factor
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    Ajikumar V Aryangat, John E Gerich
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    ABSTRACT: Hyperglycemia is a major risk factor for both the microvascular and macrovascular complications in patients with type 2 diabetes. This review summarizes the cardiovascular results of large outcomes trials in diabetes and presents new evidence on the role of hyperglycemia, with particular emphasis on postprandial hyperglycemia, in adverse cardiovascular outcomes in patients with type 2 diabetes. Treatment options, including the new dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 mimetics that primarily target postprandial hyperglycemia, are also discussed. Hyperglycemia increases cardiovascular mortality, and reducing hyperglycemia lowers cardiovascular risk parameters. Control of both fasting and postprandial hyperglycemia is necessary to achieve optimal glycated hemoglobin control. Therefore, anti-hyperglycemic agents that preferentially target postprandial hyperglycemia, along with those that preferentially target fasting hyperglycemia, are strongly suggested to optimize individual diabetes treatment strategies and reduce complications.
    Vascular Health and Risk Management 01/2010; 6:145-55.
  • Mazen Alsahli, John E. Gerich
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    ABSTRACT: As indicated earlier in Chapter 2, human plasma glucose concentrations are maintained within a relatively narrow range throughout the day (usually between 55 and 165mg/dl, ∼3.0 and 9.0mM/L) despite wide fluctuations in the delivery (e.g., meals) and removal (e.g., exercise) of glucose from the circulation. This is accomplished by a tightly linked balance between glucose production and glucose utilization regulated by complex mechanisms.
    12/2009: pages 297-312;
  • Muhammad Z. Shrayyef, John E. Gerich
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    ABSTRACT: Arterial plasma glucose values throughout a 24-h period average approximately 90mg/dl, with a maximal concentration usually not exceeding 165mg/dl such as after meal ingestion and remaining above 55mg/dl such as after exercise or a moderate fast (60h). This relative stability contrasts with the situation for other substrates such as glycerol, lactate, free fatty acids, and ketone bodies whose fluctuations are much wider (Table 2.1).
    12/2009: pages 19-35;
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    ABSTRACT: It is long known that both type 1 and type 2 diabetes can be associated with changes in gastric emptying; a number of publications have linked diabetes to delayed gastric emptying of variable severity and often with poor relationship to gastrointestinal symptomatology. In contrast, more recent studies have reported accelerated gastric emptying when adjusted for glucose concentration in patients with diabetes, indicating a reciprocal relationship between gastric emptying and ambient glucose concentrations. This review proposes that gastroparesis or gastroparesis diabeticorum, a severe condition characterized by a significant impairment of gastric emptying accompanied by severe nausea, vomiting, and malnutrition, is often overdiagnosed and not well contrasted with delays in gastric emptying. The article offers a clinically relevant definition of gastroparesis that should help differentiate this rare condition from (often asymptomatic) delays in gastric emptying. The fact that delayed gastric emptying can also be observed in non-diabetic individuals under experimental conditions in which hyperglycaemia is artificially induced suggests that a delay in gastric emptying rate when blood glucose concentrations are high is actually an appropriate physiological response to hyperglycaemia, slowing further increases in blood glucose. The article discusses the strengths and weaknesses of various methodologies for assessing gastric emptying, especially with respect to the diabetes population, and reviews newer diabetes therapies that decelerate the rate of gastric emptying. These therapies may be a beneficial tool in managing postprandial hyperglycaemia because they attenuate rapid surges in glucose concentrations by slowing the delivery of meal-derived glucose.
    Diabetes/Metabolism Research and Reviews 07/2009; 25(6):502-14. · 2.97 Impact Factor
  • Diabetes / Metabolism Reviews 06/2009; 4(1):1 - 15.
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    ABSTRACT: To assess whether an increased genetic predisposition for type 2 diabetes mellitus (T2DM) influences the contributions of insulin resistance and impaired insulin secretion to impaired glucose tolerance (IGT), 437 subjects not known to have T2DM underwent an oral glucose tolerance test and a 3-hour hyperglycemic clamp. Plasma insulin responses and insulin sensitivity were compared between all subjects (unselected for demographic or anthropometric characteristics) who had normal glucose homeostasis and no first-degree T2DM relative (n = 133), IGT with a first-degree T2DM relative (IGT/FH+, n = 74), or IGT without a first-degree T2DM relative (IGT/FH-, n = 50). Compared with those with normal glucose homeostasis, first- and second-phase plasma insulin responses were reduced approximately 45% and 30%, respectively (both P < .001), in IGT/FH+, whereas insulin sensitivity was only approximately 20% reduced (P = .011). In contrast, in IGT/FH-, first-phase plasma insulin responses were only approximately 20% reduced (P = .016), second-phase plasma insulin responses were not reduced, but insulin sensitivity was approximately 40% reduced (P < .001). The IGT/FH+ group differed significantly from the IGT/FH- group by having 25% to 30% lower first-phase plasma insulin responses (P = .026) and 25% to 30% greater insulin sensitivity (P = .027). Adjustment for obesity abolished the differences in insulin resistance but not plasma insulin responses. However, when the IGT groups were stratified into subgroups based on body mass index (BMI), first-phase plasma insulin responses were approximately 30% lower in IGT/FH+ with a BMI of at least 27 kg/m(2) (P = .018) but similar in IGT/FH+ with a BMI less than 27 kg/m(2) compared with the corresponding IGT/FH- subgroups. We conclude that, in IGT, an increased genetic predisposition for T2DM increases the contribution of impaired insulin secretion to its pathophysiology. This effect is enhanced by obesity.
    Metabolism: clinical and experimental 05/2009; 58(5):602-7. · 3.10 Impact Factor
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    ABSTRACT: To determine the efficacy and safety of liraglutide (a glucagon-like peptide-1 receptor agonist) when added to metformin and rosiglitazone in type 2 diabetes. This 26-week, double-blind, placebo-controlled, parallel-group trial randomized 533 subjects (1:1:1) to once-daily liraglutide (1.2 or 1.8 mg) or liraglutide placebo in combination with metformin (1 g twice daily) and rosiglitazone (4 mg twice daily). Subjects had type 2 diabetes, A1C 7-11% (previous oral antidiabetes drug [OAD] monotherapy >or=3 months) or 7-10% (previous OAD combination therapy >or=3 months), and BMI <or=45 kg/m(2). Mean A1C values decreased significantly more in the liraglutide groups versus placebo (mean +/- SE -1.5 +/- 0.1% for both 1.2 and 1.8 mg liraglutide and -0.5 +/- 0.1% for placebo). Fasting plasma glucose decreased by 40, 44, and 8 mg/dl for 1.2 and 1.8 mg and placebo, respectively, and 90-min postprandial glucose decreased by 47, 49, and 14 mg/dl, respectively (P < 0.001 for all liraglutide groups vs. placebo). Dose-dependent weight loss occurred with 1.2 and 1.8 mg liraglutide (1.0 +/- 0.3 and 2.0 +/- 0.3 kg, respectively) (P < 0.0001) compared with weight gain with placebo (0.6 +/- 0.3 kg). Systolic blood pressure decreased by 6.7, 5.6, and 1.1 mmHg with 1.2 and 1.8 mg liraglutide and placebo, respectively. Significant increases in C-peptide and homeostasis model assessment of beta-cell function and significant decreases in the proinsulin-to-insulin ratio occurred with liraglutide versus placebo. Minor hypoglycemia occurred more frequently with liraglutide, but there was no major hypoglycemia. Gastrointestinal adverse events were more common with liraglutide, but most occurred early and were transient. Liraglutide combined with metformin and a thiazolidinedione is a well-tolerated combination therapy for type 2 diabetes, providing significant improvements in glycemic control.
    Diabetes care 04/2009; 32(7):1224-30. · 7.74 Impact Factor
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    ABSTRACT: Coronary heart disease (CHD) risk in 20 non-diabetic women with and 20 without a distant history of gestational diabetes (hGDM), matched on age, body mass index, and time since GDM-affected pregnancy, was compared in a case control study. Women with an hGDM had lower high-density lipoprotein cholesterol (HDL-c), p = .02, and higher triglycerides, p < or = .001, versus controls. The combination of high triglycerides and low HDL-c occurred in 25% of hGDM cases versus 0% of controls, p </= .01. Two-hour post-load glucose indicated that 45% of hGDM cases were pre-diabetic versus 20% of controls, p < or = .05. Non-diabetic women with a distant hGDM are at increased risk for DM and may be at increased risk for CHD.
    Research in Nursing & Health 03/2009; 32(3):298-306. · 2.18 Impact Factor
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    ABSTRACT: Slowing of gastric emptying by hyperglycemia, a physiological response to minimize postprandial hyperglycemia, may be impaired in patients with type 1 diabetes. The causes and consequences on glucose homeostasis are unknown. Consequences of euglycemia- and hyperglycemia-induced changes in gastric emptying on postprandial glucose fluxes and excursions were studied in 10 healthy subjects and 15 type 1 diabetic subjects after ingestion of a mixed meal using the double isotope approach ([6,6-(2)H(2)] and [1-(13)C]glucose) and scintigraphic measurements of gastric emptying. Gastric emptying was greater in type 1 diabetic subjects (90-120 min, P < 0.03), and 50% retention times were comparable in healthy subjects and type 1 diabetic subjects (167 +/- 8 vs. 152 +/- 10, P = 0.32). Hyperglycemia markedly delayed gastric emptying in healthy subjects but did not alter it in type 1 diabetic subjects (50% retention time 222 +/- 18 vs. 167 +/- 8 min, P = 0.003 and 148 +/- 9 vs. 152 +/- 10 min, P = 0.51). Plasma islet amyloid polypeptide (IAPP) increased approximately fourfold in healthy subjects (P < 0.001), whereas it was undetectable in type 1 diabetic subjects. IAPP replacement, using the analog pramlintide, in type 1 diabetic subjects slowed gastric emptying to a comparable extent, as did hyperglycemia in healthy subjects (P < 0.14), and greatly reduced postprandial hyperglycemia (P < 00.1). Meal-derived glucose appearance in plasma (10.7 +/- 0.5 vs. 6.8 +/- 0.7 mumol . kg(-1) . min(-1), P < 0.001) was reduced, and splanchnic glucose sequestration increased (14.0 +/- 3.0 vs. 25.0 +/- 6.0%, P = 0.04). In patients with type 1 diabetes the ability to delay gastric emptying in response to hyperglycemia is impaired. This impairment contributes to exaggerated rates of meal-derived glucose appearance and, ultimately, postprandial glucose excursions.
    Diabetes care 01/2009; 31(12):2325-31. · 7.74 Impact Factor
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    ABSTRACT: An estimated 246 million people worldwide have diabetes. Diabetes is a leading cause of death in most developed countries, and is reaching epidemic proportions in many developing and newly industrialized nations. Poorly controlled diabetes is associated with the development of renal failure, vision loss, macrovascular diseases and amputations. Large controlled clinical trials have demonstrated that intensive treatment of diabetes can significantly decrease the development and/or progression of microvascular complications of diabetes. There appears to be no glycaemic threshold for reduction of diabetes complications; the lower the glycated haemoglobin (HbA1c), the lower the risk. The progressive relationship between plasma glucose levels and cardiovascular risk extends well below the diabetic threshold. Until recently, the predominant focus of therapy has been on lowering HbA1c levels, with a strong emphasis on fasting plasma glucose. Although control of fasting hyperglycaemia is necessary, it is usually insufficient to obtain optimal glycaemic control. A growing body of evidence suggests that reducing postmeal plasma glucose excursions is as important, or perhaps more important for achieving HbA1c goals. This guideline reviews the evidence on the harmful effects of elevated postmeal glucose and makes recommendations on its treatment, assessment and targets.
    Nutrition, metabolism, and cardiovascular diseases: NMCD 06/2008; 18(4):S17-33. · 3.52 Impact Factor

Publication Stats

13k Citations
2,876.74 Total Impact Points

Institutions

  • 1995–2014
    • University of Rochester
      • • Division of Hospital Medicine
      • • Division of Endocrinology and Metabolism
      • • Clinical Research Center (CRC)
      • • Department of Medicine
      Rochester, New York, United States
  • 2013
    • Southlake Regional Health Centre
      Bradford West Gwillimbury, Ontario, Canada
  • 2012
    • Louisiana State University Health Sciences Center New Orleans
      • Department of Medicine
      New Orleans, LA, United States
  • 2003–2009
    • University Center Rochester
      • Department of Medicine
      Rochester, Minnesota, United States
  • 1980–2009
    • Mayo Clinic - Rochester
      Rochester, Minnesota, United States
    • Washington University in St. Louis
      • Department of Medicine
      San Luis, Missouri, United States
  • 2005
    • U.S. Department of Veterans Affairs
      Washington, Washington, D.C., United States
  • 2002–2003
    • São Paulo State University
      • Faculdade de Medicina de Botucatu
      São Paulo, Estado de Sao Paulo, Brazil
  • 2000–2002
    • University Medical Center Utrecht
      Utrecht, Utrecht, Netherlands
  • 1998–2002
    • University of Tuebingen
      • Department of Ethnology
      Tübingen, Baden-Wuerttemberg, Germany
  • 1987–2002
    • University of Pittsburgh
      • School of Medicine
      Pittsburgh, PA, United States
  • 2001
    • University of North Carolina at Chapel Hill
      • Department of Medicine
      Chapel Hill, NC, United States
  • 1993
    • University of Texas Health Science Center at San Antonio
      • Division of Hospital Medicine
      San Antonio, TX, United States
    • University Hospital of North Norway
      Tromsø, Troms, Norway
  • 1988–1993
    • Università degli Studi di Perugia
      • Department of Internal Medicine
      Perugia, Umbria, Italy
  • 1980–1993
    • Mayo Foundation for Medical Education and Research
      • • Department of Pediatrics
      • • Mayo Medical School
      • • Department of Medicine
      Scottsdale, AZ, United States
  • 1989–1991
    • University of Amsterdam
      • Department of Endocrinology
      Amsterdam, North Holland, Netherlands
    • The National Institute of Diabetes and Digestive and Kidney Diseases
      Maryland, United States
  • 1990
    • Montefiore Medical Center
      New York City, New York, United States
  • 1988–1990
    • Vanderbilt University
      • Department of Medicine
      Nashville, MI, United States
  • 1984
    • University of California, Irvine
      Irvine, California, United States
  • 1981
    • University of Minnesota Rochester
      Rochester, Minnesota, United States
  • 1973–1977
    • University of California, San Francisco
      • Division of Hospital Medicine
      San Francisco, California, United States
  • 1976
    • CSU Mentor
      Long Beach, California, United States