Diabetes & Metabolism Journal

Case Report

A Case of Acromegaly Presenting with Diabetic Ketoacidosis.: Jin Dong Kim, Tae Seo Sohn, Jee In Lee, Jick Hwan Hah, Yun Hwa Jung, Jung Min Lee, Sung Min Nam, Seung Won Lee, Hyun Shik Son; Korean Diabetes J. 2006;30(4):312-315. Published online July 1, 2006; DOI: https://doi.org/10.4093/jkda.2006.30.4.312

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Abstract PDF: In patients with acromegaly, glucose intolerance and diabetes mellitus are one of the frequent manifestations. And the type of diabetes in these patients is usually non-insulin dependent type secondary to insulin resistance caused by growth hormone excess. Therefore, the diabetes mellitus in these patients dose not tend to develop diabetic ketoacidosis. But we experienced and presented the case of a patient with acromegaly hospitalized due to the diabetic ketoacidosis without overt clinical manifestations of acromegaly. This case of acromegaly showed that growth hormone excess could cause diabetic ketoacidosis in the presence of relative insulin deficiency.

Original Articles

The Effect of Growth Hormone on Insulin Resistance and Atherosclerotic Risk Factors in Obese Patients with Uncontrolled Type 2 Diabetes Mellitus.: Jae Hyun Nam, Soo Jee Yoon, Dol Mi Kim, Chul Sik Kim, Joo Young Nam, Jong Suk Park, Jina Park, Chul Woo Ahn, Suk Won Park, Bong Soo Cha, Young Duk Song, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh; Korean Diabetes J. 2003;27(2):141-152. Published online April 1, 2003

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Abstract PDF: BACKGROUND
Insulin resistance in visceral obesity constitutes a risk factor for the development of atherosclerosis. The insulin resistance in obese type 2 diabetic patients can be improved by a decrease in the visceral fat and an increase in the skeletal muscle, which may influence the insulin sensitivity. Growth hormone (GH) accelerates lipolysis and promotes protein conservation. The effects of GH therapy, with diet restriction, on lipolysis and protein anabolism, were evaluated, which may change body composition, insulin resistance and atherosclerotic risk factors in obese type 2 diabetes mellitus. METHODS: Sixteen obese type 2 diabetic patients (31~56yrs), who had high glucose levels (glucose 12.8+/-1.7 mmol/L, HbA1c 10.2+/-2.1%), were treated with recombinant human GH (GH; 1 unit/d, 5 times/week), diet restriction (25 kcal/kg ideal body weight/day) and exercise (250 kcal/day) for 12 weeks. They underwent anthropometric measurement, bioelectrical impedance for total body fat and lean body mass, as well as computed tomography, for visceral and subcutaneous fat, at the umbilicus and muscle area at the mid-thigh levels. All subjects underwent the test for GH response to hypoglycemia. The insulin sensitivity index (ISI) was measured using insulin tolerance tests (ITT). RESULTS: 1. The visceral fat area (VFA)/thigh muscle area (TMA) ratio was more decreased in the GH-treated group than in the control group, but there was no change of body weight. 2. The ISI was significantly increased in only the GH-treated group, which was negatively correlated with the VFA/TMA ratio. The serum free fatty acid, fibrinogen and plasminogen activator inhibitor-1 were significantly decreased after the GH treatment. The serum glucose level and HbA1c remained unchanged during the GH therapy, but were significantly decreased after 3 months. 3. The total cholesterol and triglyceride levels were decreased in the GH treated group. 4. The insulin-like growth factor-I, fasting c-peptide and insulin level were all significantly increased after the GH treatment. CONCLUSION: This study suggested that in type 2 diabetic patients, with insulin resistance and uncontrolled blood sugar, GH treatment caused a decrease in the visceral fat and an increase in the muscle mass, which could result in the improvement of the ISI, atherosclerotic risk factors and dyslipidemia.

Expression of ghrelin and its receptor according to feeding state in rats.: Min Seon Kim, Cho Ya Yoon, Young Joo Park, Hyung Kyu Park, Chen Ji Jin, Kyong Han Park, Chan Soo Shin, Kyong Soo Park, Seong Youn Kim, Bo Youn Cho, Hong Kyu Lee; Korean Diabetes J. 2002;26(3):169-178. Published online June 1, 2002

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Abstract PDF: BACKGROUND
Ghrelin is a newly discovered gut peptide, produced mainly in the stomach, which is secreted into the circulating blood and acts on the hypothalamus and the pituitary gland. Although ghrelin was originally identified as an endogenous growth hormone secretagogue, recent studies have suggested its role is in the regulation of food intake and energy homeostasis. The aim of this study was to investigate changes in the expression of ghrelin in the stomach, and of its receptors in the hypothalamus and the pituitary gland in relation to the feeding state. METHODS: Sprague Dawley male rats, divided into 3 groups, freely fed, fasted for 48 hrs and fasted for 48 hrs followed by feeding for 24 hrs, were investigated. The stomach fundus, the hypothalamus and the pituitary glands were collected. The gastric ghrelin mRNA expression was determined by Northern blot analysis and the ghrelin protein by immunohistochemistry. The ghrelin receptor mRNA levels in the hypothalamus and anterior pituitary gland were determined by real time PCR. RESULTS: The ghrelin mRNA levels in the stomach were increased by fasting but reduced again by allowing feeding. The number of ghrelin-immunoreactive gastric epithelial cells tended to increase with fasting. Moreover, the ghrelin receptor mRNA levels increased fold in the hypothalamus, and about 3 fold in the anterior pituitary gland harvested from the rats that had fasted for 48 hrs compared to those that were freely fed. CONCLUSION: Our data demonstrate that expression of both ghrelin in stomach and its receptor in target organs increased in the fasted state, which would be helpful for magnifying the orexigenic effect of ghrelin in the negative energy balance state. Dynamic changes in ghrelin and ghrelin receptor according to altered metabolic state may suggest a physiologic role of ghrelin in the regulation of energy homeostasis.

Changes of Insulin-like Growth Factor- I, Insulin-like Growth Factor Binding Protein-3 and 24-hour Urinary Growth Hormone in PrepubertalChildren with Insulin Dependent Diabetes Mellitus.: Choong Ho Shin, Sei Won Yang; Korean Diabetes J. 1999;23(1):25-35. Published online January 1, 2001

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Abstract PDF: BACKGROUND
The growth hormone - insulin-like growth factor-I(GH/IGF-I) axis and the insulin nutrition axis constitute two major anabolic hormone systems that interact at varous levels. It is well established that patients with type 1 diabetes mellitus have elevated GH levels and inappropriate low IGF-I for high GH levels. Such a deranged GH/IGF-I axis may complicate the somatic growth of children with diabetes. The purpose of this study assess the nature of deranged GH/IGF-I axis and the effect on somatic growth. METHODS: In the present study, serum levels of IGF-I and IGFBP-3 were measured in 31 prepubertal children with type 1 DM (age, 8.93.1yr) and were compared with those levels in children with normal short stature (control) (age, 8.4+/-2.5 yr). RESULTS: In diabetic patients, age-adjusted serum levels of IGF-I and IGFBP-3 were significantly lower than those in controls (p<0.05). The difference of serum levels of IGF-I and IGFBP-3 between diabetic patients and control increased with chronologic age. There was no difference in 24-h urinary GH (24-h uGH) excretion between diabetic patients and normal controls. Simple regression analysis reveled no correlation between height SDS (standard deviation score)and HbA, (average 7.4%), IGF-I, IGFBP-3, urinary growth hormone, and chronological age. But height SDS had a tendency to decrease with the duration of diabetes, but without statistical significance. In diabetic patients, the 24-h uGH expressed as ng/24 h was correlated with chronologic age, IGF-I, and IGFBP-3, but such correlation was not obsc:rved when the 24-h uGH was expressed as ng/g creatinine In the control group, the 24-h u(GH was expressed as ng/24 h, correlated with only IGFRP-3. CONCLUSION: The growth impairment during puberty (which may be dependent on the degree of blood glucose control), rather than during prepuberty is probably responsible for the reduced final adult height in diabetic patients. This might be partly due to a relatively good blood glucose ontrol during prepubertal period. More importantly, it is suggested that this reduced final adult height comes from a gradual decrease in IGF-I and IGFBP-3 levels for long period during diabetes, regardless of the 24-h urinary growth hormone excretion.

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