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S W Coppack

Publications and source records attributed to S W Coppack.

100 records · Page 6Linked to original sources
PubMed1989

The derivation of a minimal model insulin sensitivity index from euglycaemic clamps in man.

We describe a computer program based on the minimal model of Bergman et al., which has been used to control euglycaemic hyperinsulinaemic clamps and to derive the insulin sensitivity index (Si) from clamp data. Clamps were undertaken on 33 subjects with a range of insulin resistance. The steady state glucose had an acceptable coefficient of variation (c.v.) and was close to the desired clamp level. The c.v. of the steady state glucose infusion rate was smaller than for other clamp programmes. The Si was correlated with metabolic clearance rate for glucose (MCR) divided by the change in insulin concentration. Our results suggest that the assumptions of the minimal model hold true in the euglycaemic hyper-insulinaemic situation and demonstrate that a minimal-model-derived program can achieve acceptable clamping.

Algorithms↗
PubMed1985

Fatal varicella in a healthy young adult.

A healthy adult presented with severe neurological disturbance 4 d after developing chicken-pox. Although pneumonic and renal problems were also present the neurological state dominated the clinical picture. After the patient's sudden death an autopsy revealed that renal and cerebral problems were secondary to myocardial involvement. This was of an unusual type for varicella with features of dilated cardiomyopathy resembling that previously related to Coxsackie infections. We conclude that cardiac problems in this patient produced anoxic brain damage and subsequently death.

Adult↗
PubMedDate not supplied

The endocrine function of the fat cell-regulation by the sympathetic nervous system.

The landmark discovery of leptin established beyond question the fact that adipose tissue is a crucial active regulator of body weight, an endocrine organ in its own right and part of a feedback circuit possessing both afferent and efferent loops. This is in addition to its more established roles as a receiver of incoming endocrine signals and modulator of circulating hormones such as sex steroids. Since this discovery, much has been learned about the role of leptin in the afferent loop of the hypothalamic regulation of body weight and indeed about some of the neuro-endocrine circuitry involved in the regulation of appetite and weight. Much less, however, is known about the efferent limb of the circuit, specifically relating to how the hypothalamus is able to influence adipocyte behaviour and how this link may itself be influenced by endocrine and paracrine signals, both acting on and emanating from adipocytes themselves, acting at multiple levels. This review will focus on the role of the sympathetic nervous system (SNS) and adreno-medullary system in relation to the regulation of adipose tissue physiology and endocrine function. The evidence in support of the hypothesis that the SNS is a crucial mediator of the efferent loop of this feedback circuit will be considered.

Adipocytes↗
PubMedDate not supplied

The metabolic associations of intravenous glucose tolerance in the 10 years from diagnosis of type 2 diabetes.

Intravenous glucose tolerance was measured at diagnosis and during the subsequent 10 years in 103 Type 2 diabetic patients not treated with insulin. KG (the rate constant for clearance of intravenous glucose) was inversely related to fasting plasma glucose at all review times (at diagnosis being Rs = -0.77, p less than 0.001), and at times to the circulating concentrations of ketone bodies (at diagnosis being Rs = -0.52, p less than 0.001) and glycerol (Rs = -0.29, p less than 0.01). In the first year of treatment, most metabolic abnormalities improved. One to 10 years after diagnosis, fasting glucose concentration and intravenous glucose tolerance deteriorated (median glucose from 6.4 to 7.4 mmol l-1, p less than 0.001; median KG from 0.81 to 0.69% min-1, p less than 0.01). Likewise, the 'homeostatic model assessment' of insulin insensitivity deteriorated (median from 2.3 to 3.7 arbitrary units, p less than 0.001) over the same period but first-phase insulin secretion remained steady or improved. This suggests that increases in insulin insensitivity have a predominant effect on slowly deteriorating glucose tolerance from 1 to 10 years after diagnosis in Type 2 diabetes.

Adult↗
PubMedDate not supplied

Comparison of indices of islet B-cell function in type 2 diabetes in relation to insulin effectiveness and clinical outcome.

The most appropriate way to estimate islet B-cell function in Type 2 diabetes is unclear, and this has led to many different techniques of measurement being used. We have examined the associations to two fasting and four glucose-stimulated indices of islet B-cell function in members of a group of 249 Type 2 patients, seeking correlations with concurrent glucose tolerance and antilipolytic effect, and with subsequent clinical outcome. The six B-cell indices were interrelated to variable degrees (rs -0.21 to +0.92). Early glucose-stimulated insulin output (incremental 1st-phase insulin area) was not significantly positively correlated with the fasting plasma concentration of immunoreactive insulin at any time. Fasting immunoreactive insulin and 'minimal model' islet B-cell parameters were poorly related to the rate constant for glucose clearance and the degree of antilipolysis (rs values between -0.13 and +0.40). Homeostatic model assessment of the fasting islet B-cell function was more consistently related to these metabolic effects. Incremental first-phase insulin area was the islet B-cell index most consistently related to metabolic abnormalities (rs up to +0.56), and to subsequent need for oral hypoglycaemic or exogenous insulin therapy. No index of islet B-cell function was consistently associated with the subsequent development of diabetic tissue damage.

Aged↗