Malnutrition-related Diabetes Research Articles

Is protein‐deficient diabetes mellitus a pancreatitis?

Malnutrition-related diabetes mellitus is a distinct clinical entity subdivided into protein-deficient diabetes mellitus (PDDM) and fibrocalculus pancreatic diabetes (FCPD). Whereas FCPD has obvious pancreatitis manifested by pancreatic duct calculi, the evidence for involvement of the pancreas in PDDM is limited to the presence of ketosis-resistant hyperglycaemia. We studied 10 patients with PDDM biochemically and radiologically. Endoscopic retrograde cholangiopancreatography was performed to determine if they had any evidence of chronic pancreatitis. Their mean faecal chymotrypsin level was low (13.2+/-5.72 microg/g), as was their basal c-peptide value (0.35+/-0.15 mmol/L). Islet cell antibodies were not detected in any of these patients. Ultrasound examination revealed pancreatic atrophy. In two patients, however, the pancreas was bulky. The ERCP showed generalized thinning of the pancreatic duct, measuring 2.4+/-0.06mm in the head, 2.01+/-0.08 mm in the body and 1.02 +/- 0.03 mm in tail region; side branches were seen but they were too sparse and thin. The significance of these changes is not clear, but they may represent an ongoing pancreatic disease and may, indeed, be the earliest changes of chronic pancreatitis.

Relation between malnutrition and development of diabetes mellitus.

Obesity and increased dietary intake of high fat are considered important factors involved in the development of type 2 diabetes, as they correlate to the prevalence of diabetes in different populations and are both associated with insulin resistance, which is an important pathogenic event for diabetes (1,2). However, epidemiological studies have shown that diabetes is common also in populations where obesity is not a major concern for health (3). In fact, in some developing countries, the prevalence of diabetes exceeds that of more developed countries, as, for example, has been shown in studies in Bangladesh (4) and India (5). The question of whether also malnutrition is detrimental for glucose metabolism and may contribute to the development of diabetes has therefore been raised. This would also be supported by clinical studies showing distinct and specific clinical characteristics of diabetes in malnourished subjects when compared to nonmalnourished subjects, such as early age of onset, requirement of insulin to control hyperglycemia in conjunction with ketosis resistance in the absence of insulin therapy, and the presence of pancreatic calculi, in addition to the clinical manifestations of malnutrition (6–9). Based on these epidemiological and clinical observations, WHO recognized, in 1985, malnutrition-related diabetes mellitus (MRDM) as a special subtype of diabetes, different from type 1 (IDDM) and type 2 diabetes (NIDDM) (6). However, using malnutrition in the classification of diabetes has been questioned, because malnutrition has also been considered to be a mere coincidence with diabetes, which exaggerates or modulates the clinical feature of the disease (10,11). In fact, several arguments have been put forward against the use of MRDM as a distinct entity of diabetes. One argument is that it has not been convincingly demonstrated that malnutrition results in permanent diabetes and another argument is that the classification of diabetes into type 1 or type 2 relies on clinical aspects, not pathogenesis (6,10). In addition, malnutrition by itself is a vague condition that is difficult to define, as it is usually assessed by combined interpretation of data from the dietary history, anthropometric data, clinical examination, and laboratory investigations without strict criteria. Malnutrition is also inhomogeneous, because it includes both single and combined nutrient deficiencies as well as global energy deficiency. Moreover, the clinical characteristics thought to be specific for MRDM may also be identified in diabetic subjects without a history of malnutrition (10,12). Therefore, the new classification system of the American Diabetes Association does not consider MRDM a distinct entity of diabetes (11). Instead, fibrocalculus pancreatic diabetes (FCPD), being a former subgroup of MRDM, has been classified as an exocrine pancreatic disease, and protein-deficient diabetes mellitus (PDDM) is considered a condition modulating the clinical features of existing diabetes. Nevertheless, apart from the issue of classification, the role of malnutrition on glucose homeostasis remains elusive and needs further studies to designate it as a modulating factor in diabetes. As previously reviewed by Rao (7), malnutrition may cause diabetes as a priInternational Journal of Pancreatology, vol. 26, no. 3, 125–130, December 1999 © Copyright 1999 by Humana Press Inc. All rights of any nature whatsoever reserved. 0169-4197/99/26:125–130/$11.50

Serum and urinary magnesium in young diabetic subjects in Bangladesh

Magnesium imbalance, implicated in diabetes mellitus both as a cause and a consequence, has not yet been investigated in subgroups of subjects with malnutrition-related diabetes mellitus. which is prevalent in young patients in tropical developing countries such as Bangladesh. The present study evaluated the serum and urinary magnesium concentrations in groups of young diabetic subjects in Bangladesh. Forty patients newly diagnosed with diabetes [13 with fibrocalculus pancreatic diabetes (FCPD), 13 with protein-deficient diabetes (PDDM), and 14 with type 2 diabetes mellitus] were studied along with 13 healthy control and 13 malnourished control subjects [body mass index (in kg/m2) < 19]. Magnesium was measured by atomic absorption spectrophotometry. Malnutrition itself was not related to the serum glucose (fasting: 3.68+/-0.74 and 4.11+/-0.29 mmol/L; postprandial: 6.30+/-0.41 and 6.00+/-0.24 mmol/L for healthy and malnourished control subjects, respectively) or serum or urinary magnesium (serum: 0.73+/-0.03 and 0.75+/-0.05 mmol/L: urinary: 232+/-124 and 243+/-88 mmol Mg/mol creatinine for healthy and malnourished control subjects, respectively) concentration. Subjects with FCPD and PDDM had significantly lower serum magnesium concentrations (PDDM: 0.68+/-0.06 mmol/L, FCPD: 0.66+/-0.07 mmol/L) than those in both control groups. In contrast with 0% of healthy and 7.7% of malnourished control subjects, 42.85% of type 2 diabetic subjects, 61.54% of those with PDDM, and 69.23% of those with FCPD were hypomagnesemic. Subjects with FCPD and PDDM had significantly higher urinary excretion of magnesium than the healthy and malnourished control subjects and the type 2 diabetic subjects. Hypermagnesuria paralleled hypomagnesemia. Malnutrition may not itself give rise to glucose intolerance, and serum magnesium deficiency seems to be a consequence rather than a cause of diabetes mellitus.

Antioxidant status, oxidative stress and DNA damage in the aetiology of Malnutrition Related Diabetes Mellitus

Undernutrition is a preeminent feature of the two major clinical syndromes, protein dependent diabetes mellitus (PDDM) and fibrocalculous pancreatic diabetes (FCPD) that has been grouped together under the term malnutrition related diabetes mellitus (MRDM).[l] Although, MRDM represents only a few percent of the world population suffering from diabetes, it is a major health problem within developing countries. Investigation of these forms of the disease indicates that a genetic predisposition cannot be clearly established, and several hypotheses related to dietary-deficiency and environmental chemical exposure have been proposed. Oxidative stress induced by oxygen free radicals has been implicated in the pathogenesis of many human diseases in recent years.[2] It is becoming increasingly plausible that antioxidant deficiency leading to the exposure of pancreatic B-cells to increased oxidative stress may be implicated in the aetiology and pathogenesis of MRDM. increased oxidative stress (a high prooxidant/antioxidant ratio) which is based on evidence of increased lipid peroxidation and reduced antioxidant reserve.[3] A deficiency in the nutritional supply and availibility of antioxidants which may occur in MRDM may have consequences in terms of failure of the first line of defence against oxygen radical induced damage.[4] The aim of the study was to assess the antioxidant status and levels of oxidative stress and DNA damage in malnourished patients displaying PDDM (n=24), FCPD (n=14), non-insulin dependent diabetes mellitus (NIDDM) (n=46), and age matched controls (n=67). All diabetic patients were under 30 years and newly diagnosed to avoid complicating variables such as insulin therapy and control subjects were matched for age, BMI and socioeconomic status. Plasma vitamins A, C, and E were measured by HPLC [5,6], whilst antioxidant enzymes in red cell concentrate were measured on the Cobas Fara autoanalyser[7-10]. DNA damage within nucleated blood cells was measured using a sensitive ELISA.[11]

Islet-cell antibodies in malnutrition-related diabetes mellitus from North India

The etiology of malnutrition-related diabetes mellitus (MRDM) — protein-deficient pancreatic diabetes (PDPD) and fibro-calculous pancreatic diabetes (FCPD) — is unclear. We studied the role of autoimmunity against pancreatic islet cells in the etiology of these two subtypes of MRDM by measuring islet-cell antibodies (ICA) in 23 patients with PDPD, 25 with FCPD and 62 with Type 1 diabetes. Three patients (13%) with PDPD had detectable ICA, including a patient with a high titre of ICA (> 80 JDF units). The frequency of ICA in patients with PDPD was significantly lower than subjects with Type 1 diabetes ( 22 62 , 35%; P < 0.05). Among patients studied at onset, ICA prevalence was lower in the PDPD patients ( 1 7 , 14%) compared to subjects with Type 1 diabetes ( 8 20 , 40%). No patient of FCPD had detectable ICA ( P < 0.001 vs. Type 1 diabetes subjects). We conclude that autoimmunity may play a role in the etiology of some patients with the PDPD subtype of MRDM. However, FCPD is unlikely to have an autoimmune etiology.

Insulin resistance during euglycemic clamp studies in chronically undernourished rats with mild streptozocin diabetes

Malnutrition has been shown to impair insulin sensitivity, but it is not known whether this effect has any impact on coexisting diabetes. Insulin sensitivity was therefore studied using the glucose clamp technique in rats with chronic nutritional deprivation superimposed on mild streptozocin (STZ) diabetes mellitus. In pair-feeding experiments, 4-week-old littermate rats were either allowed ad libitum access to food or restricted to 50% of ad libitum intake for 8 weeks, and were injected with STZ 40 mg/kg intraperitoneally halfway through the experiment. Fasting plasma glucose (FPG) was similar in both groups of rats, but fasting plasma insulin (FPI) was lower in the undernourished group ( P = .016). Undernourished rats were significantly more insulin resistant during euglycemic hyperinsulinemia of the same degree, with glucose disposal rate being impaired by 50% as compared with that in ad libitum—fed diabetic littermates (24.4 ± 2.8 v 51.5 ± 4.4 μmol/kg/min, P = .0008). The insulin sensitivity index was significantly lower in the undernourished group (3.03 ± 0.32 v 5.67 ± 0.6, P = .0057). The results show that chronic undernutrition markedly reduces insulin sensitivity in rats with mild STZ diabetes. This is further evidence that chronic undernutrition is a deleterious modifying influence on coexisting diabetes mellitus. It suggests that the insulin resistance of malnutrition-related diabetes mellitus (MRDM) could potentially be an acquired defect mediated by the coexistent undernutrition, rather than a “distinctive” feature that is intrinsically unique to this diabetic syndrome.

Pancreatic pathology in non-insulin dependent diabetes (NIDDM)

NIDDM is a heterogeneous disease and subgroups of NIDDM include MODY (Maturity Onset Diabetes of the Young), Malnutrition-related diabetes (MRDM) and Fibrocalculus pancreatic diabetes (FCPD). Endocrine cell population is relatively unchanged in NIDDM: B-cells are reduced by up to 30% and A-cells increased by 10%. Islet amyloid is found in 96% of subjects occupying up to 80% of the islet associated with a reduction in B-cells. Amyloid formation is unlikely to cause diabetes but progressive accumulation increases the severity of the disease. Islet amyloid is formed from the islet amyloid polypeptide (IAPP), a normal constituent of B-cells, co-secreted with insulin. The causal factors for IAPP fibrillogenesis are unknown but abnormal synthesis or overproduction could be involved: stimulation of B-cell secretion in NIDDM by obesity, hyperglycaemia or suphonylurea therapy may promote amyloidosis and further aggravate islet pathology. A mutation of the glucokinase gene in MODY leads to diminished B-cell secretion but not amyloid formation. Diabetes and mutations of mitochondrial DNA is associated with poorly developed islet structure. Exocrine pancreatic size is reduced and there is evidence of sub-clinical chronic pancreatitis in NIDDM. In MRDM and FCPD, chronic pancreatitis and exocrine necrosis is associated with reduced insulin secretion. Unlike cystic fibrosis where islet amyloid is present in diabetic individuals, amyloid is absent from subjects with FCPD. Pathological changes in the exocrine and endocrine pancreas in NIDDM results from and contributes to the pathophysiology of insulin secretion in NIDDM.

A study of thyroid function and prevalence of thyroid autoantibodies in an African diabetic population

It is generally believed that autoimmune disorders are uncommon in Africans. Some workers have argued that insulin-dependent diabetes mellitus (IDDM) is rare in Africa on account of this reduced proneness to autoimmunity. However, it is undetermined whether or not Africans with IDDM have increased prevalence of thyroid dysfunction and autoimmunity, two phenomena strongly associated with Caucasian IDDM. We determined thyroid function and the prevalence of thyroid autoimmunity in IDDM Africans. The results are compared with those of a nondiabetic group and a group with non-insulin-dependent diabetes mellitus (NIDDM). Thyroid hormone levels were significantly lower in IDDM patients than in the control population and the NIDDM population. Subclinical hypothyroidism was present in 21% of the 28 IDDM patients. One patient was hypothyroid and another hyperthyroid. Of the 60 NIDDM patients, 5 (8.3%) had subclinical hypothyroidism. Forty-six percent of the IDDM patients had significant levels of serum thyroid autoantibodies (TAAB). This was significantly higher than the 1.4% and 1.7%, respectively, in the controls and NIDDMs. Presence of TAAB in the patients was strongly associated with thyroid dysfunction, female preponderance, and duration of diabetes mellitus. Thyroid dysfunction and autoimmunity are common in Nigerians clinically diagnosed as IDDM, and have prevalence rates comparable to other populations but higher than rates previously reported from some other African groups. The increased prevalence of thyroid autoimmunity in the IDDM supports the view that these patients are true IDDMs rather than variants of NIDDM or malnutrition-related diabetes mellitus (MRDM) as has been suggested by some workers.

Fibrocalculous Pancreatic Diabetes in Pune, India: Clinical features and follow-up for 7 yr

To study clinical features of fibrocalculous pancreatic diabetes from this clinic, to compare these with the published criteria of malnutrition-related diabetes mellitus, and to conduct serial follow-up of these patients to study difficulties in their treatment. Details of presenting symptoms, anthropometry, diabetic tissue damage, treatment, and follow-up of 55 patients with fibrocalculous pancreatic diabetes (pancreatic calculi demonstrated on X-ray and sonography) treated during the last 7 yr were studied. Many patients did not fit the accepted criteria of malnutrition-related diabetes. Thus, 17 (31%) were diagnosed after 30 yr of age and 23 (42%) had a body mass index > 18 kg/m2, and the daily dose of insulin in these patients (mean 0.8 U/kg) was similar to that in the IDDM patients (mean 1.0 U/kg). The two pathognomonic complaints (pancreatic pain and steatorrhea) were not always present. Many patients took very irregular treatment, but none suffered diabetic ketoacidosis despite stopping insulin for long periods of time; 33% of patients had some diabetic tissue damage when first seen. Fourteen patients were lost to follow-up, and 11 died during the follow-up. Clinical features of these fibrocalculous pancreatic diabetes patients were somewhat different than the classic descriptions. A need exists to reconsider classification of FCPD under malnutrition-related diabetes mellitus. Many patients receive irregular treatment, and a substantial proportion die within a few years of diagnosis, many as a result of preventable causes.

A search for malnutrition-related diabetes mellitus among Ethiopian patients.

To search for evidence of MRDM among Ethiopian patients. We reviewed the records from March 1976 to January 1991 of 1835 Ethiopian diabetic patients registered consecutively in the Diabetic Clinic of Yekatit 12 Hospital in Addis Ababa, Ethiopia. Of those aged 15-30 at onset, 41.3% had a BMI < 19 kg/m2 at diagnosis, and 55% of the latter had a history of normal weight before the onset of symptoms. The frequency of KA was similar in the very thin patients and others of the same age-group, and only 1 patient required > 1.5 IU insulin in 24 h. Pancreatic calcification was observed in only 4 middle-aged men with histories of alcohol abuse, and the very thin patients did not have other stigmata of malnutrition. Of the 1604 patients > or = 18 yr of age at diagnosis, only 21 of 1116 who knew their previous weight had a BMI < 19 kg/m2 before the onset of diabetic symptoms, and most of the 178 patients with a BMI < 19 kg/m2 on treatment had been normal or even overweight. In regression analysis, the factors associated with weight loss before diagnosis were the duration of symptoms in type I diabetes patients and the need for insulin from diagnosis, poverty certification, and symptom duration in type II diabetes patients. Weight gain with treatment was related to female sex, the duration of symptoms, and the absence of tuberculosis in type I diabetes patients and related to an address/birthplace not in Addis Ababa in type II diabetes patients. The undernutrition at presentation is probably caused by the untreated diabetic state and is reversible with treatment, even if the patient is poor and/or lives in a rural area. No convincing cases of MRDM fulfilling the published definition could be found.

Persistent reduction of pancreatic beta-cell mass after a limited period of protein-energy malnutrition in the young rat.

Kwashiorkor, the human disease of protein-energy malnutrition, has been implicated in the aetiology of malnutrition-related diabetes mellitus, a form of diabetes not uncommon in developing countries. We have previously demonstrated that temporary protein-energy malnutrition in young rats causes a persisting impairment of insulin secretion. The present study investigates whether this secretory deficiency is accompanied by structural alterations of the endocrine pancreas. Three-week-old rats were weaned onto semi-synthetic diets containing either 15% or 5% protein and these diets were maintained for 3 weeks. From 6 weeks of age all rats were fed a commercial chow containing 18% protein. The endocrine pancreas was investigated by light and electron microscopic morphometry at 3, 6 and 12 weeks of age. In rats not subjected to protein-energy malnutrition there was a progressive increase, with age, of total pancreatic Beta-cell weight and individual Beta-cell size. In 6-week-old rats fed the low protein diet total pancreatic Beta-cell weight and individual Beta-cell size were diminished. In 12-week-old rats previously fed the low protein diet total Beta-cell weight remained lower compared to control rats. It is concluded that protein-energy malnutrition early in life may result in a diminished reserve for insulin production. This may predispose to glucose intolerance or even diabetes in situations with an increased insulin demand.

Immunogenetic and nutritional profile in insulin-using youth-onset diabetics in Korea

There are few reports on the genetic, immunological and nutritional characteristics of insulin-using youth-onset diabetes mellitus, insulin-dependent diabetes mellitus (IDDM) and malnutrition-related diabetes mellitus (MRDM) in Korea. Among 1266 hospitalized Korean diabetics, 29 (2.3%) were IDDM and 84 (6.6%) were MRDM. A diabetes history of first-relatives (28.6%) was more frequently found in the MRDM group than in the IDDM (14.8) and non-insulin-dependent diabetes mellitus (NIDDM) (19.0%) groups. HLA-DR4 was more common among IDDM (54.2%) and MRDM (52.4%) patients than controls (26.3%), and HLA-DR3 was more common among only IDDM patients (29.2%) than controls (10.9%). Conventional islet-cell antibodies were detected in 8 of 15 IDDM patients tested (53.3%) and in 11 of 22 MRDM patients (50.0%). MRDM patients had higher serum basal (1.02 ± 0.51 ng/ml) and peak (1.44 ± 0.76 ng/ml) C-peptide concentrations than IDDM patients, but lower concentrations than NIDDM patients. Before the onset of diabetes, the calorie intake of 21 MRDM patients assessed was 63.1% of the daily requirement and the intake of carbohydrate, protein and fat was 71.7%, 55.9% and 39.8%, respectively. In summary, our data suggest that IDDM in Korea is associated with HLA-DR3 or HLA-DR4, indicating a risk for IDDM in Western societies; furthermore, MRDM has a history of undernutrition at the preonset period and is also associated with HLA-DR4. It might be also concluded that MRDM in Korea is another expression of IDDM caused by the shortage of some nutrients for the structural and/or functional maintenance of pancreatic β-cells.

Diabetes Mellitus in Saudi Arabia: The Clinical Pattern and Complications in 1,000 Patients

A retrospective and prospective study of 1,000 ambulatory and hospitalized diabetic patients was done in Riyadh, Saudi Arabia. Saudis completed 777 (77.7%) and non-Saudis 223 (22.3%). Sex distribution was equal among Saudis, males 389 (50.1%) and females 388 (49.9%), but non-Saudi males were predominant at 153 (68.6%), non-Saudi females 70 (31.4%) reflecting the preponderant male expatriate labor force. A proportion of different types of diabetes was: IDDM 115 (11.7%), non-obese non-insulin dependent diabetes mellitus (NIDDM) 405 (41.0%), obese NIDDM 412 (42.1%), and early onset non-insulin dependent diabetes (diagnosis under 30 years of age), 43 (4.4%). Regarding treatment, 388 (40.6%) received insulin followed by sulfonylurea, alone in 330 (33.5%), diet only 117 (12.0%), combination sulfonylurea and biguanide in 113 (11.6%), biguanide alone in 13 (1.3%) and insulin plus tablets in 7 (0.8%). Of 472 and 426 patients, 29.7% and 30.0% had elevated total cholesterol or triglycerides respectively, while 77.2% of 373 patients had elevated glycosylated hemoglobin (HbA1). At least once in 998 patients, diabetic ketoacidosis occurred in 7.6%.

Chronic Undernutrition Accentuates Insulin Deficiency in Rats With Mild Streptozocin-Induced Diabetes

The effect of chronic undernutrition on coexisting diabetes mellitus was studied in pair-fed littermate rats with mild streptozocin-induced diabetes. They were either fed ad libitum or 50% food restricted for 9 wk. Undernourished diabetic rats, in which weight gain was reduced by 40%, had significantly higher glucose intolerance (mean +/- SE, fractional rate of glucose disappearance during glucose tolerance test [Kgtt] 1.77 +/- 0.16) than diabetic littermates fed ad libitum (2.33 +/- 0.21, P less than 0.05) or nondiabetic controls (3.8 +/- 0.7, P less than 0.01). The total area under the insulin response curve was significantly reduced in both groups of diabetic rats, but the undernourished group showed a 45% greater reduction in overall secretion than normally nourished diabetic littermates (21.3 +/- 2.7 vs. 39.4 +/- 6.3 nM.min in the diabetic group, P less than 0.01, and 65.7 +/- 6.1 nM.min in controls). There was also a marked reduction in first-phase insulin secretion in the undernourished rats (4.75 +/- 0.24 vs. 9.84 +/- 1.36 nM, P less than 0.05, and 14.3 +/- 1.8 nM, P less than 0.01, respectively, in normally nourished diabetic littermates and controls). After refeeding, a significant improvement occurred in Kgtt (to 2.67 +/- 0.24, P less than 0.01) and first-phase insulin secretion (to 9.69 +/- 1.65 nM, P less than 0.05). The postrefeeding values were not different from those in the normally nourished diabetic littermates, indicating that the effect was fully reversible and solely attributable to undernutrition rather than to enhanced beta-cell cytotoxicity from streptozocin.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevalence, age at diagnosis, clinical characteristics and treatment of diabetes in the young in Pahang, Malaysia

The prevalence, age at diagnosis, clinical characteristics and treatment of young diabetics, younger than 40 years were determined on the basis of a cross-sectional study of medical records of 2 health districts in Pahang, Malaysia. There were only 20 insulin-dependent diabetics (IDDM), prevalence 0.07 per 1000 inhabitants. There were 84 non-insulin-dependent diabetics (NIDDM), prevalence 0.3 per 1000 inhabitants. Three of the NIDDM patients could have malnutrition-related diabetes. Many NIDDM patients were asymptomatic which is an important reason why many of them remain undetected in the community. Seventy-four percent of the patients below the age of 30 years at diagnosis had NIDDM, 56% of the patients below the age of 20 years at diagnosis also had NIDDM and 54% of the NIDDM patients had a strong family history of diabetes. Many NIDDM patients were misdiagnosed as IDDM, especially if they were underweight, leading to considerable overuse of insulin. This study confirms that IDDM is rare in Malaysia, as in other Asian countries. Most young diabetics have NIDDM and have a strong family history. This pattern of diabetes in the young is unlike that seen in the West.

Insulin and Glycaemic Response to Common Carbohydrate Diets in Undernourished Diabetics

Nearly 30% of diabetics in India are undernourished (UND) and have to consume a higher calorie diet where the bulk comes from cereal-based carbohydrates (CHO). In Orissa, parboiled rice, flaked rice (chuda) and broken cream of wheat (suji) are most commonly used. Glycaemic and insulinogenic responses to these were assessed in six patients, each with malnutrition-related diabetes (MRDM), and six undernourished non insulin-dependent diabetics (lean NIDDM), along with 10 healthy controls. Serum levels of insulin (IRI), both basal and in response to glucose, were lowest in MRDM. In spite of severe hyperglycaemia, IRI values in lean NIDDM were more or less similar to controls, indicating a high degree of insulin resistance in the former. Insulin glucose indices (IG index) were lowest in MRDM. In controls, the glycaemic index (GI) of rice was lowest (43.8±11.6) as compared with chuda (74.9±11.1) and suji (64.9±20.3). In UND rice showed higher GI compared with controls, and suji and chuda even higher GI. However...

Anthropometric studies in diabetes in the Tropics

Anthropometric studies were carried out in three groups of diabetics seen in southern India, namely fibrocalculous pancreatic diabetes (FCPD) (n = 49) (a subtype of malnutrition related diabetes), insulin dependent diabetes mellitus (IDDM) (n = 55) and non-insulin dependent diabetes mellitus (NIDDM) (n = 104). Both FCPD and IDDM had significantly lower body mass index, skinfold thickness (triceps, biceps, subscapular and suprailiac), mid-arm circumference and fat mass compared to controls and NIDDM patients, (p less than 0.001 for all parameters). FCPD and IDDM males did not show any significant differences in any of the anthropometric parameters studied. Among the females, FCPD had lower triceps skinfold measurements (p = 0.007) and mid-arm circumferences (p less than 0.05) compared to IDDM patients. Patients with NIDDM did not show any significant difference compared to the control group. This study shows that both FCPD and IDDM patients have lower body mass and fat mass compared to NIDDM patients and control subjects.

Prevalence and clinical features of diabetes mellitus secondary to chronic pancreatitis in Japan; a study by questionnaire

The prevalence and clinical features of diagnosed diabetes mellitus secondary to chronic pancreatitis (CP) were assessed from northern (Hokkaido) to southern (Okinawa) Japan by means of a questionnaire to elucidate whether WHO-classified malnutrition-related diabetes mellitus (MRDM) exists in Japan. Of a total 17 500 diabetic patients, only two (0.011%) — one fibrocalculous pancreatic diabetes (FCPD) and one protein-deficient pancreatic diabetes (PDPD) — exhibited MRDM characteristics. A total of 649 CP were collected and classified into 268 cases with chronic alcoholic pancreatitis (CAP), 150 cases with chronic calcified pancreatitis (CCP) and 231 cases with other CP. The prevalence of diabetes mellitus was found to be 50.7% in CAP, 72.7% in CCP and 22.8% in other CP. Among all diabetics, 56.6% was noninsulin-dependent (NIDDM) and 26.4% insulin-dependent (IDDM). IDDM was most frequent in CP. Satisfactory and less than satisfactory glycemic control was obtained in approximately three quarters of all subjects. Only one quarter showed poor glycemic control. Insulin treatment was frequent in CAP (52.2%) and CCP (61.7%), but less in other CP (27.5%). The prevalence of diabetic retinopathy was observed in 33.1% of all subjects, nephropathy 21.0% and neuropathy 36.3%, respectively. The prevalence of complications, including macroangiopathy tended to be higher in CAP and CCP (40.3 and 56.9%) than in other CP (31.4%).

The clinical and hormonal (C-peptide and glucagon) profile and liability to ketoacidosis during nutritional rehabilitation in Ethiopian patients with malnutrition-related diabetes mellitus

Cases of malnutrition-related diabetes mellitus conforming to the description of the protein deficient pancreatic diabetes type in Ethiopian patients were compared with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic. Fourteen of 39 malnutrition-related diabetes mellitus patients had fat malabsorption compared with only two of ten Type 1 diabetic patients and one of nine control subjects. Xylose absorption was normal favouring a pancreatic cause for the malabsorption. Plasma C-peptide during oral glucose tolerance test was significantly lower than that in Type 2 diabetic patients and normal control subjects (p less than 0.01 to 0.001) and was also consistently but not significantly higher than in Type 1 diabetic patients. Glucagon secretion patterns were similar in malnutrition-related and Type 1 diabetic patients. Of 23 new malnutrition-related diabetic patients treated with glibenclamide after nutritional rehabilitation and insulin treatment, only three responded, 14 were unresponsive but remained ketosis free for over eight days while another six developed ketoacidosis or significant ketonuria within two to six days during the trial. Sixteen unselected Type 1 diabetic patients who discontinued their insulin therapy all developed frank ketoacidosis after a mean of 5.5 days. The similarity of the malnutrition-related and Type 1 diabetes mellitus in age of onset, insulin requirement for diabetic control and appearance of ketosis-proneness in some cases, together with the similarity of C-peptide and glucagon secretion patterns suggest that the protein deficient pancreatic diabetes variant of malnutrition-related diabetes mellitus may be Type 1 diabetes mellitus modified by the background of malnutrition rather than an aetiologically separate entity.(ABSTRACT TRUNCATED AT 250 WORDS)

HLA-DR and -DQ antigens in malnutrition-related diabetes mellitus in Ethiopians: a clue to its etiology?

Thirty Ethiopian malnutrition-related diabetes mellitus (MRDM) patients were HLA typed and their HLA antigen frequencies were compared to those of 31 previously typed insulin-dependent diabetes mellitus (IDDM) patients and to 84 controls from the same ethnic background. In comparison to controls, a striking association between MRDM and HLA-DR3 (X2 = 15.15, p = 0.0001) was observed, whereas the frequency of HLA-DR4 was non-significantly increased (RR = 1.72). The frequency of DR2, DQw1, and DQw6 was decreased among MRDM. In comparison to IDDM that is associated with both DR3 and DR4 in this population, MRDM showed no significant differences in HLA class II antigens frequencies. Therefore, the genetic basis of susceptibility to MRDM and IDMM in Ethiopia is at least partially identical.