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"LATAR BELAKANG. Progresifitas penurunan sekresi insulin sudah terjadi sebelum individu didiagnosis sebaai DM tipe-2 baru karena kelelahan sel beta pankreas untuk mengatasi resistensi insulin. Efek glukotoksisitas, Iipotoksisitas dan amiloidosis pada sel beta pankreas menyebabkan proses tersebut terus berlanjut walaupun pasien telah diterapi dengan baik. Berbagai penelitian memperlihatkan sebagian besar penyandang DM tipe-2 baru ditemukan dengan fungsi sel beta pankreas yang sudah rendah. Populasi tersebut lebih cepat mengalami kegagalan terapi dibandingkan populasi dengan fungsi sel beta pankreas yang masih baik akibat progresifitas penurunan sekresi insulin yang lebih cepat, sedangkan resistensi insulin dalam tingkatan yang sama. Akibatnya prevalensi kegagalan mencapai kontrol glukosa darah yang baik menjadi tinggi pada populasi tersebut, dan merupakan salah satu penyebab komplikasi makrovaskular maupun mikrovaskular yang semakin meningkat. Di poliklinik diabetes RSCM dan berbagai puskesrnas di Jakarta, sebagian besar penyandang DM tipe-2 sulit untuk mencapai kontrol glukosa darah yang baik dan tingginya prevalensi komplikasi makrovaskular maupun mikrovaskular. Apakah populasi tersebut sudah berada dalam fungsi sel beta pankreas yang rendah? Penelitian ¡ni bertujuan untuk mengetahui gambaran fungsi sel beta pankreas melaluiperhitungan HOMA-B dan resistensi insulin melalui perhitungan HOMA-IR padasubyek penyandang DM tipe-2 baru yang berobat di poliklinik diabetes RSCM.METODOLOGI. Dirancang studi potong lintang dengan analisis deskriptif. Prosedur yang dilakukan adalah subyek dipuasakan selama 10 jam lalu diperiksa konsentrasi glukosa darah puasa dan insulin puasa. Dari hasil tersebut dilakukan penghitungan HOMA-B dan HOMA-IR.HASIL. Telah dilakukan pengambilan data terhadap 100 subyek. Nilai median usia 52 tahun. 51% dan subyek mempunyai riwayat keluarga DM dan sebagian besar subyek adalah obes sebanyak 54%. Sebagian besar subyek dalam kelompok nilai HOMA-B yang sangat rendah yaitu kurang dari 25 pmol/mmol sebanyak 55% dengan nilai median 17,14 pmol/mmol, dan dalam kelompok nilai HOMA-IR yang rendah yaitu kurang dari 3 pmol-mmol/l2 scbanyak 61% dengan niai median 245 pmol-mmol/l2.SIMPULAN. Sebagian besar penyandang DM tipe-2 baru di poliklinik diabetes RSCM adalah obes dan manpunyai riwayat keluarga DM. Sebagian besar subyek berada dalam kelompok fungsi sel beta pankreas dan resistensi insulin yang rendah.

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BACKGROUND. The declining of insulin secretion already happened before the patent diagnosed type 2 diabetic, caused by beta cell pancreas failure in order to compensate insulin resistance. The glucotoxicity and lipotoxicity effect combined with amyloidosis onì beta cell pancreas caused continuing declining process progessiveIy even though the patient has been treated. Most of the previous studies showed that many new type 2 diabetic patients have already had low beta cell finction. This population failed to achieve targeted therapy faster than population with good beta cell function, because faster the declining of insulin secretion. However, innsulin resistance was almost constant. Because of that, prevalence of failed to achieve good blood glucose control were high and one of the mechanisms cause micro and macro vascular complication will increase. Many type 2 diabetic who attended in endocrine metabolic clinic in Cipto Mangunkusumo hospital and Primary Health Care in Jakarta failed to achieve good blood glucose control and there were high incidence of macro and micro vascular complication We hypothesized that many new type 2 diabetIc patients in endocrine metabolic clinic in Cipto Mangunkusumo have already had low beta cells function. We investigated the profile of beta cells function by calculated IIOMA-13 and insulin resistance by calculated ROMA-IR in new type 2 diabetic patients who attenckxl in endocrine metabolic clinic ¡n Cipto Mangunkusumo hospital.METHOD. A descriptive-cross sectional study was conducted. After 10 hours fasting, new type 2 diabetic patients were checked for fasting blood glucose and fasting insulin concentration. Based on those numbei, The HOMA-B and HOMA-IR were calculated.RESULT. Based on the results of 100 patients. Median value of age was 52 years old. 51% of the subjects had family history of diabetic and most of them were obese in 54% subjects. Most of the subjects were in lower HOMA-B value less than 25 Pmol/mmol in 55% of the subiects with median NOMA-B vahe was 17,14 pmol/mmol and wese in lower HOMA-IR less than 3 pmol-mmol,I2 in 61% of the subjects with median HOMA-ER value was 2,45 pmol-mmol/12 groups.CONCLUSION. Many new type 2 diabetic patients, who attended in endocrine metabolic Clinic in Cipto Mangunkusumo hospital, were obese and have already had family history of diabetic. Most of the subjects were in low pancreas beta cell function and insulin resistance groups."

"Latar belakang: Hormon tiroid berperan dalam regulasi metabolisme glukosa. Kondisi hipertiroid menyebabkan perubahan fungsi sel beta pankreas, percepatan pengosongan lambung, dan gangguan absorpsi glukosa di usus yang menyebabkan kelainan metabolisme glukosa hingga terjadinya resistensi insulin dan disfungsi sel beta pankreas. Tujuan: Mengetahui korelasi kadar hormon tiroid dengan resistensi insulin dan disfungsi sel beta pankreas pada pasien penyakit Graves fase toksik. Metode: Penelitian ini menggunakan desain potong lintang untuk menilai HOMA-IR dan HOMA-B pada pasien penyakit Graves fase toksik. Penelitian dilakukan di RS Cipto Mangunkusumo dari Januari 2019 hingga Agustus 2020. Kriteria inklusi penelitian ini yaitu pasien penyakit Graves usia 18-65 tahun, belum menerima terapi obat antitiroid atau sudah diberikan terapi obat selama maksimal 1 bulan dan masih dalam fase toksik. Analisis data menggunakan korelasi Pearson. Hasil: Dari total 38 pasien dengan kecurigaan penyakit Graves, 2 pasien dieksklusi dari penelitian karena hasil TRAb negatif. Pada studi ini ditemukan bahwa tidak terdapat korelasi antara kadar T4 bebas dengan resistensi insulin (r 0,208 ; p 0,298) dan disfungsi sel beta pankreas (r 0,215 ; p 0,928) pada pasien penyakit Graves fase toksik. Tidak ditemukan juga korelasi antara TSH dan T3 total dengan resistensi insulin dan disfungsi sel beta pankreas. Didapatkan korelasi yang kuat dan bermakna antara HOMA-IR dan HOMA-B (r 0,991 ; p 0.000). Kesimpulan: Tidak didapatkan korelasi antara kadar hormon tiroid (T4 bebas, T3 total, dan TSH) dengan resistensi insulin dan disfungsi sel beta pankreas.

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Background: Thyroid hormones play a significant role in glucose metabolism. Hyperthyroid cause changes in pancreatic beta cell function, accelerated gastric emptying, and impaired glucose absorption in the intestine which cause abnormality in glucose metabolism, resulting in insulin resistance and pancreatic beta cell dysfunction. Aim: To determine correlation of thyroid hormone with insulin resistance and pancreatic beta cell dysfunction in toxic phase Graves’ disease patients. Method: This study is a cross-sectional study to assess HOMA-IR and HOMA-B in toxic phase Graves’ disease patients. The research was conducted at Cipto Mangunkusomo Hospital from January 2019 to August 2020. Inclusion criteria for this study were Graves’ disease patients aged 18-65 years, never received anti-thyroid medication or anti-thyroid medication had been given for maximum of 1 month and patient still in the toxic phase. Data analysis used Pearson correlation. Results: From 38 patients suspected with Graves’ disease, 2 patients were excluded from the study because of negative TRAb results. This study found there was no correlation between free T4 levels and insulin resistance (r 0,208; p 0,298) and pancreatic beta cell dysfunction (r 0,215; p 0,928) in toxic phase Graves’ disease patients. There was also no correlation found between TSH and total T3 with insulin resistance and pancreatic beta cell dysfunction. A strong and significant correlation was found between HOMA-IR and HOMA-B (r 0,991; p 0.000). Conclusion: There was no correlation between thyroid hormone (free T4, total T3, and TSH) and insulin resistance. Thyroid hormones also did not correlate with pancreatic beta cell dysfunction."

"Latar Belakang: Diabetes melitus (DM) tipe 2 awitan muda memiliki karakteristik patofisiologi yang khas, termasuk disfungsi sel β yang lebih cepat dan resistensi insulin yang menonjol, terutama pada kondisi obesitas. Lipotoksisitas, akibat akumulasi lemak ektopik dan gangguan fungsi jaringan adiposa, diketahui berperan dalam terjadinya resistensi insulin dan disfungsi sel β. Namun, peran lipotoksisitas pada DM tipe 2 awitan muda belum banyak diteliti. Tujuan: Mengetahui hubungan antara lipotoksisitas, yang dinilai melalui visceral adiposity index (VAI) dan lipid accumulation product (LAP), dengan resistensi insulin (homeostasis model assessment of insulin resistance; HOMA-IR) dan fungsi sel β (homeostasis model assessment of β-cell function; HOMA-β) pada pasien DM tipe 2 awitan muda. Metode: Penelitian ini merupakan studi potong lintang yang menggunakan data dasar dari registri studi Genomik di RS Cipto Mangunkusumo (September 2022–Desember 2023). Subjek penelitian sebanyak 135 pasien DM tipe 2 dengan usia awitan ≤40 tahun dan tidak menggunakan insulin. VAI dan LAP dihitung berdasarkan data antropometri dan biokimia. HOMA-IR dan HOMA-β dihitung dari kadar glukosa dan insulin puasa. Analisis korelasi dan regresi linier berganda dilakukan dengan penyesuaian faktor perancu. Hasil: VAI dan LAP menunjukkan korelasi positif signifikan dengan HOMA-IR (r = 0,33 dan r = 0,47; p < 0,001), yang mencerminkan korelasi lemah hingga sedang dengan resistensi insulin. Faktor-faktor selain lipotoksisitas kemungkinan berkontribusi terhadap proses resistensi insulin. Tidak ditemukan korelasi signifikan antara VAI maupun LAP dengan HOMA-β. Analisis multivariat menunjukkan bahwa hubungan antara VAI/LAP dengan HOMA-IR tidak dipengaruhi oleh jenis kelamin, durasi DM, riwayat keluarga, kadar LDL, atau obat antidiabetes. Simpulan: Lipotoksisitas yang dinilai melalui VAI dan LAP berkorelasi dengan resistensi insulin, namun tidak dengan disfungsi sel β pada DM tipe 2 awitan muda.

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Background: Early-onset type 2 diabetes mellitus (T2DM) presents distinct pathophysiological characteristics, including accelerated β-cell dysfunction and prominent insulin resistance, often in the context of obesity. Lipotoxicity, resulting from ectopic fat accumulation and impaired adipose tissue function, is believed to contribute to both insulin resistance and β-cell dysfunction. However, its role in early-onset T2DM remains understudied.

Objective To examine the association between lipotoxicity, assessed by visceral adiposity index (VAI) and lipid accumulation product (LAP), with insulin resistance (homeostasis model assessment of insulin resistance; HOMA-IR) and β- cell function (homeostasis model assessment of β-cell function; HOMA-β) in patients with early-onset T2DM.

Methods: This was a cross-sectional study using baseline data from the Genomic Study registry at Dr. Cipto Mangunkusumo Hospital (September 2022–December 2023). Subjects included 135 patients diagnosed with T2DM at age ≤40 years and not on insulin therapy. VAI and LAP were calculated from anthropometric and biochemical parameters. HOMA-IR and HOMA-β were derived from fasting glucose and insulin levels. Correlation and multiple linear regression analyses were conducted, adjusting for potential confounders.

Results: VAI and LAP showed significant positive correlations with HOMA-IR (r = 0.33 and r = 0.47, respectively; p < 0.001), indicating a weak and moderate correlation with insulin resistance. Factors other than lipotoxicity may contribute to the development of insulin resistance. No significant correlations were found between either VAI or LAP and HOMA-β. Multivariate analysis showed that the associations between VAI/LAP and HOMA-IR were not confounded by sex, diabetes duration, family history, LDL levels, or antidiabetic medications.

Conclusions: Lipotoxicity, as assessed by VAI and LAP, is associated with insulin resistance but not β-cell dysfunction in early-onset T2DM."