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Foetal and infant growth and Type 2 diabetes
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Starting from. Only 3 left. Add to Cart. Technical specifications. Compatibility Chart. Description 16mm female adapter. As pointed out 19 it is probable that des 31, 32 or des 64, 65 are the main products in plasma but for simplicity the term 32—33 split is used here. Another possibility that arose from this work was that 32—33 split proinsulin might have a pathogenic significance.
We return to the interpretation of this finding below. Although the finding of a uniformly reduced early insulin response to oral glucose in Type 2 diabetic subjects seemed to be received as something of a shock a couple of years ago, review of the literature of obesity-controlled studies over the years shows this to be an almost universal finding e. Disagreement over the insulin status of Type 2 diabetic subjects has often resulted from the use of different aspects of the plasma insulin response to oral glucose to assess status.
Emphasis has been variously placed on the early insulin response, the 2 h insulin concentration or the area under the insulin curve or a combination of these. It is now clear that the early insulin response is of critical importance in determining glucose tolerance. Studies of subjects with impaired glucose tolerance [IGT] give less clear cut findings than in Type 2 diabetes, but provide little evidence of universally raised early insulin responses as might be expected of a condition which has been suggested to be largely determined by insulin resistance e.
Studies such as those listed above however cannot determine whether insulin deficiency, insulin resistance or a combination of the two leads to Type 2 diabetes. A large prospective study of adult men and women living in Ely, Cambridgeshire, UK, has been initiated to address this issue.
An early and surprising finding to emerge from this work is that there is in this population a continuous relationship between height and glucose tolerance and that both men and women subjects with impaired glucose tolerance are significantly shorter than matched control subjects.
Previous work by one of us DJPB has led to the conclusion that cardiovascular disease in adult life results from restraint of growth during foetal life and infancy. Programming may be defined as a permanent or long-term change in the structure or function of an organism resulting from a stimulus or insult acting at a critical period of early life. This link was subsequently demonstrated in studies of individual men and women whose foetal and infant growth was recorded at the time.
The first study was carried out in the county of Hertfordshire, England, where since all babies born have been weighed at birth and at one year. Among men those who had the lowest weight at birth and at one year had the highest death rates from ischaemic heart disease as adults. This posed the question of what processes link lower rates of foetal and infant growth with cardiovascular disease.
Subsequent studies in Hertfordshire and in the city of Preston showed that lower birthweight, especially if associated with disproportionately high placental weight, is linked to raised blood pressure in adult life and to elevated plasma levels of fibrinogen.
Poor maternal nutrition was suggested as an important environmental influence. The known associations of Type 2 diabetes and IGT with ischaemic heart disease and hypertension 45 , 46 plus awareness of the rapid growth of Beta cells during foetal life 47 suggested to us that reduced glucose tolerance may be another outcome of early growth restraint. Of the Hertfordshire men who still live in the county attended for venous blood sampling in the fasting state. Of these men agreed to have a full 75 g oral glucose tolerance test.
From this study some strong relationships have emerged. Forty three percent of men with weights at one year of 8. It is possible that some infants with heavier birth weights were the outcome of pregnancies complicated by gestational diabetes. However, the number of such babies would have been small and their survival 60 or more years ago would probably have been poor.
Though there is evidence that gestational diabetes predisposes to diabetes in the offspring, 49 this could not explain our findings that the largest babies are those least likely to develop diabetes. Analysis of the effects of obesity, measured as body-mass index, showed that its diabetogenic effect adds to that of poor early growth.
The mean 2-h glucose concentration ranged from 5. Interestingly there was a similar addition of the effects of obesity and low weight at one year on current fasting 32—33 split proinsulin concentration.
The extremes of the range defined as above were 2. When the subjects were divided into quintiles according to the fasting 32—33 split proinsulin concentration this measurement was highly correlated with systolic blood pressure Table 1. This association is consistent with earlier findings linking 32—33 split proinsulin and risk factors for ischaemic heart disease 22 and requires an explanation. Relationship of 32—33 split proinsulin to systolic blood pressure in men aged 59—70 years.
The concentrations of 32—33 split proinsulin measured in the Hertfordshire study are in the low pmolar range. Any biological activity of this derivative at these low concentrations has yet to be described. He has hypothesised that insulin resistance is the underlying factor linking these phenomena. Our data suggests a different interpretation. Consistent with previous findings 43 blood pressure in the Hertfordshire men was inversely related to birth weight though unlike 2-h plasma glucose it was not related to weight at one year.
Our working hypothesis is that the varying components and combinations of Syndrome X, possibly including insulin resistance, are late outcomes of abnormal growth and development processes occurring in foetal and early infant life. At first sight it may seem improbable that events occurring in the first 2 years of existence could produce changes 50—70 years later. However looked at in another way it is perhaps less surprising.
It has been calculated that the fertilised ovum in developing into a full-term infant goes through some 42 rounds of cell division. The number of these divisions and their timing in development varies widely between different tissues.
For example at birth a virtually full complement of brain neurons and of renal glomeruli are present and, available data suggest, at the age of 1 year at least half the adult complement of Beta cells is present.
Poor intrauterine nutrition may lead either to generalised growth retardation, or growth of the brain may be protected at the expense of the viscera. Evidence for selective growth retardation comes from the studies of blood pressure in Preston, UK where one group of people with high blood pressure as adults was characteristed at birth by their shortness in relation to their head circumference.
Poor foetal nutrition may be caused by poor maternal nutrition A link with poor maternal nutrition would explain the high rates of impaired glucose tolerance and diabetes in parts of the third world and is also consistent with the occurrence of Type 2 diabetes in more affluent countries. Thus we propose that poor nutrition of the foetus and infant leads to permanent changes of the structure and function of certain organs and tissues.
The timing and precise nature of the deficiencies determine the pattern of metabolic and functional abnormalities seen in later life, including diabetes and hypertension and possibly also including some hyperlipidaemias and even insulin resistance. We suggest that poor early development of islets of Langerhans and Beta cells is a major factor in the aetiology of Type 2 diabetes.
In referring to poor early development we do not at this stage consider this necessarily to be a solely quantitative deficiency of Beta cells but include the possibility that the cells themselves may be altered, or that the more complex aspects of islet structure and function, such as vasculature 54 and innervation may be abnormally developed. Therefore major changes in islet vasculature such as have been described 54 could make a large contribution to changes in islet and particularly Beta cell function.
Many of the histological studies which have been carried out thus far have failed to control for the effects of obesity on Beta cells. However, as reviewed by Kloppel and colleagues, 55 there is now a general consensus that the number and total area of islets are reduced, mainly due to a decrease in the volume of Beta cells. A recent paper from the University of Minnesota pancreas transplant programme showed that even hemipancreatectomy in humans leads to a considerable deterioration of insulin secretion and glucose tolerance.
The early insulin response was virtually arithmetically halved in these subjects and 7 out of 28 developed severely abnormal glucose tolerance. In parallel with this data, work from Weir's laboratory has shown that careful quantitation of the degree of deficiency produced by pancreatic ablation in animals is needed.
Both after neonatal streptozotocin and pancreatectomy considerable regeneration of Beta cells occurs in the rat. Our assertion that poor foetal growth is associated with Type 2 diabetes in later life begs the question:. Many studies have shown the key role of amino acids in foetal growth. Not only are they essential for laying down the protein required by the growing foetus but interestingly they are also a major source of substrate for energy production.
The availability of amino acids may be monitored by the Beta cell, just as the Beta cell senses the availability of nutrients in the adult. Thus, it is important to understand what effect amino acids have on the development and growth of Beta cells in the foetus and also whether they control foetal insulin secretion.
Evidence available to date strongly suggests that amino acids are the major factors controlling Beta-cell growth and development and insulin secretion until late foetal life.
Glucose has little effect until late gestation. If the key sequence of events is the supply of amino acids leading to insulin secretion leading to foetal growth then we should ask:. A recent collaborative study between Milan and Denver has shown that this is indeed the case and that the deficiency is large.
If a major cause of defective intrauterine and early post natal growth is linked to insulin deficiency and this in turn leads to adult diabetes, then we should be able to show that there is defective production and performance of Beta cells in this situation and that such defects are irreversible. James and Coore studied treated malnourished children and suggested that they showed a permanent reduction of insulin response to glucose. He even questioned whether this might predispose to adult diabetes.
Certainly there is evidence of a major effect of intrauterine malnutrition. Growth retarded new born infants have reduced numbers of Beta cells and reduced insulin secretion. An explanation of the discrepancy between the deficit of Beta cells and the severe loss of insulin secretion may lie in the finding that protein deficiency not only reduced Beta cells mass but produced an even larger effect on islet vascularisation.
Indeed one cannot help wondering whether poor vascularisation might lead to poor clearance of insoluble peptides. Or in other words could amyloid deposition be secondary to vascular changes? This would of course have an accelerating effect on the underlying pathology. In addition underfeeding young rats lowers adult plasma insulin. This is not restored by refeeding normally. Work in the s and early s showed clearly that a failure of early cell multiplication leads to an irrecoverable deficit in cell numbers.
In reviewing the effect of poor foetal and early postnatal nutrition on Beta-cell growth and function we have placed great emphasis on the role of protein and amino acids. We have done this because there is considerable evidence that, as far as insulin production is concerned, protein and amino acid supply are critically important.
However, optimum nutrition in pregnancy and early life depends on a complex interaction of many nutrients concerning which we are still largely ignorant. How do we reconcile the view which we are putting forward with the widely accepted theory that Type 2 diabetes is totally genetically determined? In the first place the mechanisms we propose by no means exclude genetically based changes. We do suggest however that in thinking of candidate genes in Type 2 diabetes we should widen our horizons considerably and consider genes involved in foetal growth and development.
The evidence that we have presented raises a question about the interpretation of concordance in identical twin data. A genetic interpretation of concordance rates of Type 2 diabetes in identical twins may not be justifiable since identical twins share a common early nutritional environment. The familial pattern of Type 2 diabetes may have a similar explanation Family members share a similar socio-economic environment, which is known to be linked to the incidence and prevalence of Type 2 diabetes.
The stronger maternal than paternal influence on the development of Type 2 diabetes 73 is consistent with our hypothesis. So too are the results of a large genetic study of Type 2 diabetes. Instead it was discovered that the strongest influence was the common environment shared by the siblings.
We propose that Type 2 diabetes is the outcome of the foetus and early infant having to be nutritionally thrifty. This thrift results in impaired growth of the Beta cells and the islets of Langerhans.
As long as the individual persists in the undernourished state there is no need to produce much insulin. However, a sudden move to good or over-nutrition exposes the reduced state of Beta-cell function and diabetes results. This situation was demonstrated recently in the Ethiopian Jews transported to Israel among whom a high prevalence of diabetes was observed The effect of a rapid transition from subsistence to good or overnutrition was also seen in the Nauruan islanders who suffered severe nutritional deficiency before and during the last World War.
After the war, they became affluent from phosphate mining. Diabetes on the island became epidemic. An interesting consequence of what we are suggesting is that the advent of good nutrition should start to result in better infant and foetal growth which in turn will reduce the incidence of diabetes, provided always of course that the population does not become fatter and less active. It was therefore interesting to see the outcome of the most recent survey of the islanders.
The authors attributed this to a eugenic affect of lower reproduction of diabetic subjects. However, the size and speed of the improvement makes this explanation unlikely. We suggest it was due to a great improvement of foetal and infant nutrition consequent upon post-war affluence. Thus, infants born after are now up to 46 years old. It was among them that the reduction in diabetes was seen.
The essence of the hypothesis is that poor nutrition in foetal and early infant life are detrimental to the development and function of the Beta cells of the islets of Langerhans. Such defects of structure and function, which may include more complex features of islet anatomy such as the vasculature and innervation, predispose to the later development of Type 2 diabetes.
Existing evidence points to a key role for protein and amino acids in this process but other nutritional defects are not excluded. Whilst these early changes powerfully determine susceptibility, additional factors such as obesity, ageing, physical inactivity, and possibly other processes leading to insulin resistance must also play a role in deciding the time of onset and severity of Type 2 diabetes Figure 1.
Also outlined is the suggestion that the features of Syndrome X 49 may have closely related origins in failures of early growth and development.