Islet Cell Replication and Diabetes

Hellerström, Claes; Swenne, Ingemar; Andersson, Arne

doi:10.1007/978-3-642-72691-0_9

Cited by 64 publications

(52 citation statements)

References 139 publications

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“…However, replication per se has not been evaluated in the present study. As expected (see Hellman 1959, Saito et al 1978, Hellerström et al 1988, islet cell mass was higher in the splenic portion of the pancreas in Wistar rats. This pattern of distribution was also present in hybrid and GK rats.…”

Section: Discussionsupporting

confidence: 86%

Lack of compensatory increase in islet blood flow and islet mass in GK rats following 60% partial pancreatectomy

Svensson

Östenson²,

Bodin³

et al. 2005

Journal of Endocrinology

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The effects of a 60% partial pancreatectomy were studied in hyperglycemic GK (Goto-Kakizaki) rats. Partial pancreatectomy or a sham operation was performed on 12-weekold female Wistar rats, GK rats or hybrids between male GK rats and female Wistar rats. Measurements of pancreatic blood flow and islet blood flow were performed by a microsphere technique 2 weeks after surgery. Glucose tolerance was decreased in hybrid compared with Wistar rats, and in GK rats compared with both hybrid and Wistar rats before surgery. Partial pancreatectomy induced minor changes in glucose tolerance. Wistar rats had a decreased islet mass following partial pancreatectomy. Both hybrid and GK rats showed a significant decrease in relative islet volume, but only GK rats in total islet mass, compared with Wistar rats 2 weeks after surgery. Pancreatic blood flow and islet blood flow did not significantly differ between sham-operated Wistar, hybrid or GK rats. After partial pancreatectomy, islet blood flow in relation to islet mass increased 3-fold in Wistar rats and 2-fold in hybrid rats. In contrast, GK rats showed no increase in islet blood flow following partial pancreatectomy. It is concluded that compensatory mechanisms after partial pancreatectomy are operating less efficiently in hybrid and GK rats.

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Section: Discussionsupporting

confidence: 86%

Lack of compensatory increase in islet blood flow and islet mass in GK rats following 60% partial pancreatectomy

Svensson

Östenson²,

Bodin³

et al. 2005

Journal of Endocrinology

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“…Neogenesis has been stimulated experimentally (6)(7)(8)(9)(10)(11) and is seen in normal postnatal development (12,13). Quantification of neogenesis has been difficult but has usually been achieved by distinguishing between extra-islet and intra-islet endocrine cells (10,14).…”

Section: Assessment Tools For ␤-Cell Turnovermentioning

confidence: 99%

“…Compilation of data from male Sprague-Dawley rats showed that there was an increase in ␤-cell mass with age from birth until 6-10 months (13), with a linear increase from about 1 month (weaning) until 6 months; a recent study (18) shows that in Lewis rats, the ␤-cell mass continues to increase even up to 20 months of age. With even a 2-3% proliferation, the ␤-cell mass would almost double within 1 month if there were no cell loss (12). If the cell loss equaled the cell renewal, there could be complete replacement in 1 month.…”

Section: Evidence Of ␤-Cell Turnovermentioning

confidence: 99%

beta-cell turnover: its assessment and implications.

2001

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The pancreatic ␤-cells are responsible for the maintenance of the body's glucose levels within a very narrow range; their population is dynamic and undergoes compensatory changes to maintain euglycemia. The structural parameters that allow mass changes (replication, neogenesis, cell volume changes, and cell death) can now be assessed and have proved to be powerful tools. Changes in one parameter can dramatically affect the ␤-cell mass. Unfortunately, conclusions are often drawn on measurements that do not assess ␤-cell mass but only relative volumes. Throughout the lifetime of a mammal, low levels of ␤-cell replication and apoptosis are balanced and result in a slowly increasing mass. The balance allows gradual replacement of the ␤-cell population; thus, ␤-cells should be considered a slowly renewed tissue. Two major implications of ␤-cell turnover are that 1) at any time, the ␤-cells would be at different ages and 2) any limitation on replacement could have dire consequences for glucose homeostasis. Diabetes 50 (Suppl. 1):S20-S24, 2001 T he evidence that the ␤-cell mass exists in a dynamic state is becoming increasingly strong. Accumulated experimental data from rodents show that ␤-cells change in mass and function to maintain plasma glucose levels in a very narrow range. The structural parameters that allow mass changes (replication, neogenesis, cell volume changes, and cell death) have been recognized for many years, but only in the last decade have integrated analyses of these parameters been done. From these studies, several concepts have emerged:• There is growth of the ␤-cell mass throughout the life span.• There is continued renewal and loss, that is, turnover, of ␤-cells.• There exist additional compensatory changes to maintain glucose homeostasis. This perspective will address the basis of these concepts, address the assessment of the components that regulate ␤-cell mass and turnover, and discuss the implications of having a slowly renewed and ever-expanding ␤-cell mass. ASSESSMENT TOOLS FOR ␤-CELL TURNOVERTo be able to document ␤-cell turnover, there are a number of parameters one must quantitate: ␤-cell mass, ␤-cell number, and ␤-cell replication. Two other parameters, ␤-cell neogenesis and ␤-cell apoptosis, can be documented for frequency, but rates for these cannot as yet be measured.The assessment of ␤-cell mass has proved to be a powerful tool. Unfortunately, often conclusions have been drawn on measurements that do not assess ␤-cell mass but only relative volumes. To estimate ␤-cell mass, one must have the pancreatic weight as well as quantitate the relative volume (also called relative density, volume density, or percentage of pancreatic tissue) of the ␤-cells. The pancreatic weight can be equated with pancreatic volume or mass if one makes the reasonable assumption that 1 cm 3 tissue weighs 1 g. With data for relative volume and pancreatic weight, one can estimate the absolute weight or mass of the ␤-cells (Fig. 1). Many different methods for quantitating the relative volume of a tissue exi...

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“…There are conflicting reports on whether the P-cell mass is reduced in subjects with noninsulin-dependent diabetes (107). As a working hypothesis it seems reasonable to propose that nutritional and other factors determining fetal and infant growth influence the size and function of the adult pancreatic P-cell complement.…”

Section: Insulin Deficiencymentioning

confidence: 99%

Fetal, Infant, and Childhood Growth Are Predictors of Coronary Heart Disease, Diabetes, and Hypertension in Adult Men and Women

Osmond¹,

Barker²

2000

Environmental Health Perspectives

145

130

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Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. These programmed changes may be the origins of a number of diseases in later life, including coronary heart disease, hypertension and noninsulindependent diabetes. We review epidemiologic studies in which the incidence of these diseases has been related to the recorded, early growth of individuals, while considering factors in the adult lifestyle, such as obesity and socioeconomic status. We discuss possible mechanisms. For hypertension these mechanisms include placentation, maternal blood pressure, fetal undernutrition; childhood growth, activation of the renin-angiotensin system, renal structure, programming of the hypothalamic-pituitary-adrenal axis, vascular structure, and sympathetic nervous activity. For noninsulin-dependent diabetes we discuss mechanisms concerning both insulin resistance and insulin deficiency. We include a review of evidence for the programming of serum cholesterol and clotting factor concentrations. We address the timing of critical windows for coronary heart disease, reviewing studies that allow assessment of the relative importance of fetal, infant, and childhood growth. We argue for a research strategy that combines clinical, animal, and epidemiological studies.

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Islet Cell Replication and Diabetes

Cited by 64 publications

References 139 publications

Lack of compensatory increase in islet blood flow and islet mass in GK rats following 60% partial pancreatectomy

Lack of compensatory increase in islet blood flow and islet mass in GK rats following 60% partial pancreatectomy

beta-cell turnover: its assessment and implications.

Fetal, Infant, and Childhood Growth Are Predictors of Coronary Heart Disease, Diabetes, and Hypertension in Adult Men and Women

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