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8. Adiponectin stimulates glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase

Author

Yamauchi, T., Kamon, J., Minokoshi, Y., Ito, Y., Waki, H., Uchida, S., Yamashita, S., Noda, M., Kita, S., Ueki, K., Eto, K., Akanuma, Y., Froguel, P., Foufelle, F., Ferre, P., Carling, D., Kimura, S., Nagai, R., Kahn, B.B., and Kadowaki, T.

Abstract

Adiponectin (Ad) is a hormone secreted by adipocytes that regulates energy homeostasis and glucose and lipid metabolism. However, the signaling pathways that mediate the metabolic effects of Ad remain poorly identified. Here we show that phosphorylation and activation of the 5'-AMP-activated protein kinase (AMPK) are stimulated with globular and full-length Ad in skeletal muscle and only with full-length Ad in the liver. In parallel with its activation of AMPK, Ad stimulates phosphorylation of acetyl coenzyme A carboxylase (ACC), fatty-acid oxidation, glucose uptake and lactate production in myocytes, phosphorylation of ACC and reduction of molecules involved in gluconeogenesis in the liver, and reduction of glucose levels in vivo. Blocking AMPK activation by dominant-negative mutant inhibits each of these effects, indicating that stimulation of glucose utilization and fatty-acid oxidation by Ad occurs through activation of AMPK. Our data may provide a novel paradigm that an adipocyte-derived antidiabetic hormone, Ad, activates AMPK, thereby directly regulating glucose metabolism and insulin sensitivity in vitro and in vivo., Author(s): T. Yamauchi [1, 2, 8]; J. Kamon [1, 8]; Y. Minokoshi [3]; Y. Ito [1]; H. Waki [1, 2]; S. Uchida [1]; S. Yamashita [1]; M. Noda [2, 4]; [...]

Published
2002
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9. The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity

Author

Yamauchi, T., Kamon, J., Waki, H., Terauchi, Y., Kubota, N., Hara, K., Mori, Y., Ide, T., Murakami, K., Tsuboyama-Kasaoka, N., Ezaki, O., Akanuma, Y., Gavrilova, O., Vinson, C., Reitman, M.L., Kagechika, H., Shudo, K., Yoda, M., Nakano, Y., Tobe, K., Nagai, R., Kimura, S., Tomita, M., Froguel, P., and Kadowaki, T.

Abstract

Adiponectin is an adipocyte-derived hormone. Recent genome-wide scans have mapped a susceptibility locus for type 2 diabetes and metabolic syndrome to chromosome 3q27, where the gene encoding adiponectin is located. Here we show that decreased expression of adiponectin correlates with insulin resistance in mouse models of altered insulin sensitivity. Adiponectin decreases insulin resistance by decreasing triglyceride content in muscle and liver in obese mice. This effect results from increased expression of molecules involved in both fatty-acid combustion and energy dissipation in muscle. Moreover, insulin resistance in lipoatrophic mice was completely reversed by the combination of physiological doses of adiponectin and leptin, but only partially by either adiponectin or leptin alone. We conclude that decreased adiponectin is implicated in the development of insulin resistance in mouse models of both obesity and lipoatrophy. These data also indicate that the replenishment of adiponectin might provide a novel treatment modality for insulin resistance and type 2 diabetes., Author(s): T. Yamauchi [1]; J. Kamon [1]; H. Waki [1]; Y. Terauchi [1]; N. Kubota [1]; K. Hara [1]; Y. Mori [2]; T. Ide [3]; K. Murakami [3]; N. Tsuboyama-Kasaoka [...]

Published
2001
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22. General Lectures

Author

Yamaoka, Y., Nagai, T., Furuta, K., Inagawa, T., Sugiya, T., Kai, T., Amamoto, H., Okunara, T., Miyoshi, A., Araya, S., Sometani, T., Ogura, T., Yamato, T., Hirata, S., Hashimoto, T., Hamanaka, Y., Shakudo, Y., Ozaki, T., Noda, S., Kobayashi, K., Sasaki, K., Matsuura, R., Ueno, H., Ito, T., Umayahara, A., Koga, Y., Watanabe, K., Nabeya, K., Shimura, I., Ohyama, O., Komatsuzaki, T., Ogoshi, K., Hara, Y., Hiratsuka, H., Kubo, N., Masuda, H., Inoue, S., Arakawa, H., Koizumi, K., Mukozima, K., Inoue, Y., Hosaka, H., Kikuchi, N., Yoshida, H., Sakumoto, I., Inaba, M., Yokoi, Y., Abei, T., Iwama, S., Shirota, A., Miki, M., Ōkawa, K., Onda, M., Yoshioka, M., Shiba, T., Yamashita, K., Moriyama, Y., Adachi, K., Miyashita, M., Henmi, H., Egami, K., Toi, K., Fukiwake, T., Ito, H., Tamesue, N., Ohsato, K., Nagamitsu, S., Nishimura, M., Yamashita, Y., Yao, T., Mizuno, S., Tanabe, M., Yanase, M., Suzuki, K., Suzuki, K., Hayashi, K., Nishitani, T., Katake, K., Iwasa, N., Nishimura, S., Miyoshi, M., Fukumoto, K., Fujii, H., Inatomi, I., Nakajima, H., Hojo, Y., Tosaka, T., Kaneko, H., Yoshikawa, K., Mori, K., Uematsu, T., Takahashi, T., Morikawa, S., Hashi, M., Sakamoto, T., Kimura, A., Sasagawa, T., Maeda, Y., Matsukawa, M., Aizawa, T., Tabata, I., Munakata, A., Toda, S., Tajima, T., Matsunaga, F., Ogata, T., Nakayama, K., Nakayama, T., Minota, S., Otani, A., Takei, S., Tanaka, M., Miki, H., Hojo, K., Hirota, E., Sano, R., Murashima, Y., Okuuti, Y., Miwa, K., Suga, T., Yaosaka, T., Namiki, M., Kawauti, H., Nakagawa, K., Kasukawa, T., Kobayashi, S., Watanabe, H., Yamagata, S., Narasaka, T., Imai, H., Tsuneoka, T., Watanabe, H., Hoshi, K., Nishiyama, S., Hoshi, K., Fushimi, I., Hirai, T., Katsuda, M., Hirose, M., Yokomori, H., Matsumoto, T., Watanabe, N., Matsuura, K., Ishibashi, T., Nakata, S., Takei, C., Asano, H., Miyoshi, H., Hidaka, T., Dodo, H., Kitada, A., Nakamura, T., Sakata, S., Kitamura, S., Nakamua, T., Sakata, S., Kitamura, S., Agata, E., Aikawa, K., Oshima, A., Fujimoto, I., Kobayashi, T., Asakawa, Y., Kusakari, M., Abe, C., Tarumi, S., Yamashita, T., Takasu, S., Komase, Y., Hamada, H., Shoji, F., Saito, S., Takayama, T., Fujita, R., Kumura, F., Umeda, K., Okamoto, S., Nishio, H., Shintani, Y., Saitoh, K., Tatara, T., Iwamiya, K., Tamura, M., Tamura, K., Nakano, A., Tamura, U., Nakajima, T., Ichioka, G., Takeuchi, Y., Ayada, K., Torisu, R., Kamada, H., Matuoka, R., Turuoka, M., Sagara, Y., Nakamura, S., Sakasita, O., Mashimo, N., Sekiguchi, T., Kobayashi, S., Kishimoto, H., Takeuchi, T., Murakami, S., Koga, S., Ueno, M., Nishizawa, M., Nomoto, K., Kariya, A., Hayashi, M., Kobayashi, S., Mizuno, K., Mayama, S., Shinozuka, T., Maruyama, T., Ogiwara, T., Okui, K., Higurashi, K., Ito, T., Miyata, Y., Tamura, T., Ikeda, S., Nakata, J., Oshima, H., Mori, S., Otsuka, Y., Oki, I., Tasaka, S., Yamahatsu, J., Inaba, E., Sanada, K., Oura, T., Kinoshita, T., Akagi, M., Katsuhisa, F., Misumi, A., Urashima, K., Ninomiya, S., Hukami, M., Mori, T., Matsuo, Y., Seki, A., Kitamura, T., Mori, H., Yokota, R., Kawashima, S., Itoshima, T., Shimada, Y., Itoshima, T., Inoue, T., Fukuhara, J., Kubota, M., Ohta, W., Ohta, W., Kagaya, T., Abe, R., Kai, Y., Katono, S., Komatsu, K., Masuda, H., Inoue, S., Arakawa, H., Hamajima, T., Kitamura, T., Nakagawa, F., Tamura, H., Kiyonaga, G., Inui, H., Asai, H., Hayashi, N., Obata, H., Toki, F., Kakae, U., Yamauchi, D., Hisamitsu, T., Aziki, K., Tamiya, M., Watanabe, S., Kurokawa, K., Takemoto, T., Murakami, S., Kessoku, Y., Kuwana, H., Hino, K., Kato, A., Ito, A., Arakawa, Y., Ohono, Y., Hase, M., Ariga, K., Usui, R., Kutsukake, S., Nagamori, S., Nagano, H., Shimano, K., Ohya, T., Kikuchi, S., Ito, M., Hidano, S., Banno, H., Tomura, A., Kato, K., Koyama, T., Komatsu, T., Takei, T., Tomimura, K., Yamauchi, M., Sato, G., Sato, R., Haga, M., Toyokawa, S., Yamamoto, J., Ohtomi, S., Ishibashi, Y., Fukuda, M., Endo, R., Ueno, Y., Hisamitsu, T., Sasaki, T., Kobayashi, C., Kusakari, T., Yajima, T., Maeda, M., Kotoda, K., Okuda, K., Ariga, H., Takazawa, G., Nakamura, Y., Ohbayashi, A., Mitsui, H., Nakata, K., Suematsu, T., Kashiwagi, T., Hayashi, N., Baba, T., Tobimatsu, Y., Kamada, T., Abe, H., Matsuoka, K., Matsushima, S., Kamisaka, Y., Kitsuki, T., Ohnuki, H., Fujii, M., Inoue, R., Yamamoto, T., Wakisaka, G., Nakagawa, S., Nagata, K., Takebayashi, J., Nagashima, H., Tanaka, N., Kanai, K., Oda, T., Katayama, T., Furukawa, Y., Miyasaki, R., Noguchi, M., Hirose, K., Maezawa, H., Kano, H., Hirano, K., Ogino, M., Nishiwaki, K., Aoki, T., Morishita, T., Funatsu, K., Morita, A., Okazaki, I., Matsuzaki, S., Oda, M., Asakura, H., Kamegaya, K., Tsuchiya, M., Sambe, K., Kawakami, H., Kunimasa, T., Aimitsu, A., Yamashita, S., Miyoshi, A., Enzan, H., Ikehara, K., Shiozaki, Y., Sameshima, Y., Mizuno, T., Sasakawa, M., Nagi, S., Nagata, T., Fuwa, H., Tatsumi, K., Komatsu, K., Ozeki, T., Kaneda, M., Otsuki, M., Tadaki, H., Miura, K., Yamagata, S., Iwamura, K., Yamanaka, I., Sugimoto, E., Yamazaki, Y., Shiraishi, I., Yamanaka, T., Koike, H., Shimura, S., Hirayama, Y., Nishikawa, H., Kawamura, T., Kamiyama, Y., Takeda, H., Kamano, Y., Kitamura, O., Yamaoka, Y., Nanbu, H., Ozawa, K., Takasan, H., Honjo, I., Itakura, H., Akanuma, Y., Kagaya, T., Kaito, I., Sato, S., Sahara, H., Arisue, T., Kashimura, K., Motoyama, W., Hayashi, H., Okuyama, S., Ito, S., Inagaki, T., Kato, Y., Kakumu, S., Kurokawa, S., Yamawaki, T., Kusakabe, A., Hara, T., Funayama, A., Takahashi, T., Furuta, S., Omori, A., Hanaoka, S., Nagata, A., Tsukioka, J., Kiyosawa, K., Akahane, Y., Koike, Y., Oda, M., Tanaka, K., Kojima, M., Kawaguchi, Y., Kimura, A., Osamura, H., Kurihara, N., Okabe, K., Fujisawa, K., Takahashi, T., Kitami, N., Namihisa, T., Yamaguchi, K., Hisauchi, T., Nambu, M., Iijima, K., Rin, K., Kuroda, H., Kobayashi, N., Inami, Y., Shiga, K., Kon, T., Yamada, T., Yamada, T., Mizoguchi, Y., Enomoto, T., Monna, T., Yamamoto, S., Morisawa, S., Imoto, S., Uchita, K., Yamasawa, Y., Hiraide, S., Hikita, G., Takatsuki, K., Okimoto, Y., Nakagawa, J., Ito, K., Hirayama, C., Kawasaki, H., Irisa, T., Arimura, K., Amagase, H., Shibasaki, K., Tashiro, S., Ichida, F., Tozawa, T., Ishii, M., Inoue, E., Ikehara, H., Baba, S., Miyaji, Y., Nakajima, K., Shimizu, T., Shimizu, Y., Ohnishi, S., Sasaki, S., Kinami, Y., Mizukami, T., Nishida, Y., Nakagawa, T., Ojima, T., Takeshita, Y., Yamashita, T., Furuto, T., Ono, T., Yamaguchi, K., Mizuno, S., Tsumori, K., Miyagi, K., Suga, Y., Tatsumi, S., Kitano, A., Makiishi, H., Mitani, E., Mohri, S., Kamata, T., Kobayashi, K., Yamamoto, S., Yoshii, T., Takemoto, T., Suzuki, H., Hiratsuka, H., Takada, K., Maruyama, M., Takemoto, T., Suzuki, H., Katsu, K., Nomura, M., Kiyama, T., Hirabayashi, H., Yamashita, H., Masuyama, S., Takehara, Y., Sato, T., Abe, H., Sugiura, M., Shima, F., Ichihara, S., Yamasaki, Z., Fukuzawa, S., Horiguchi, Y., Takeda, T., Nakano, S., Kitamura, K., Miwa, M., Suzuke, T., Okada, K., Nakamura, T., Kikuchi, T., Mishima, K., Mandai, M., Kondo, H., Yamagata, Y., Uchida, Y., Harada, H., Nishizawa, M., Nomoto, K., Kariya, A., Ueno, M., Hayashi, M., Kobayashi, S., Mizuno, K., Shinozuka, T., Maruyama, T., Ogiwara, T., Okui, K., Miyake, N., Okada, M., Takahashi, K., Koizumi, H., Hayashi, T., Maeda, H., Abe, M., Takahashi, I., Matsumoto, M., Unoura, T., Iwasaki, A., Hattori, T., Tanaka, M., Hara, T., Sato, H., Hirashima, T., Shioda, A., Kawamura, I., Muto, M., Tsuchiya, R., Sato, Y., Ozawa, T., Hatano, T., Arae, H., Sekine, T., Tsukamoto, M., Shiratori, T., Asaki, S., Oba, E., Yamagata, H., Kobiyama, M., Hisamichi, S., Kitagawa, M., Kobayashi, N., Kurosawa, T., Tokimatsu, S., Kawasaki, S., Iwasa, A., Nagashima, K., Kodeki, K., Hoshizawa, T., Murakami, H., Yagi, T., Matsuda, T., Iwazaki, T., Suzuki, Y., Taketomi, H., Akaike, Y., Naramoto, J., Tsuru, T., Inoue, M., Nagase, T., Kato, K., and Kohyama, K.

Published
1973
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23. Aging and diabetes mellitus

Author

Akanuma Y

Subjects
Adult, Blood Glucose, Male, Gerontology, Aging, business.industry, Middle Aged, medicine.disease, Text mining, Diabetes mellitus, Diabetes Mellitus, medicine, Humans, Insulin, Female, Geriatrics and Gerontology, business, Aged
Published
1991

24. Diabetic Retinopathy and Microalbuminuria Can Predict Macroalbuminuria and Renal Function Decline in Japanese Type 2 Diabetic Patients: Japan Diabetes Complications Study

Author

Moriya, T, Tanaka, S, Kawasaki, R, Ohashi, Y, Akanuma, Y, Yamada, N, Sone, H, Yamashita, H, Katayama, S, Moriya, T, Tanaka, S, Kawasaki, R, Ohashi, Y, Akanuma, Y, Yamada, N, Sone, H, Yamashita, H, and Katayama, S

Abstract

OBJECTIVE: To examine the interactive relationship between diabetic retinopathy (DR) and diabetic nephropathy (DN) in type 2 diabetic patients and to elucidate the role of DR and microalbuminuria on the onset of macroalbuminuria and renal function decline. RESEARCH DESIGN AND METHODS: We explored the effects of DR and microalbuminuria on the progression of DN from normoalbuminuria and low microalbuminuria (<150 mg/gCr) to macroalbuminuria or renal function decline in the Japan Diabetes Complications Study (JDCS), which is a nationwide randomized controlled study of type 2 diabetic patients focusing on lifestyle modification. Patients were divided into four groups according to presence or absence of DR and MA: normoalbuminuria without DR [NA(DR-)] (n = 773), normoalbuminuria with DR [NA(DR+)] (n = 279), microalbuminuria without DR [MA(DR-)] (n = 277), and microalbuminuria with DR [MA(DR+)] (n = 146). Basal urinary albumin-to-creatinine ratio and DR status were determined at baseline and followed for a median of 8.0 years. RESULTS: Annual incidence rates of macroalbuminuria were 1.6/1,000 person-years (9 incidences), 3.9/1,000 person-years (8 incidences), 18.4/1,000 person-years (34 incidences), and 22.1/1,000 person-years (22 incidences) in the four groups, respectively. Multivariate-adjusted hazard ratios of the progression to macroalbuminuria were 2.48 (95% CI 0.94-6.50; P = 0.07), 10.40 (4.91-22.03; P < 0.01), and 11.55 (5.24-25.45; P < 0.01) in NA(DR+), MA(DR-), and MA(DR+), respectively, in comparison with NA(DR-). Decline in estimated glomerular filtration rate (GFR) per year was two to three times faster in MA(DR+) (-1.92 mL/min/1.73 m(2)/year) than in the other groups. CONCLUSIONS: In normo- and low microalbuminuric Japanese type 2 diabetic patients, presence of microalbuminuria at baseline was associated with higher risk of macroalbuminuria in 8 years. Patients with microalbuminuria and DR showed the fastest GFR decline. Albuminuria and DR should be consider

Published
2013

35. Non-insulin-dependent Diabetes Mellitus (NIDDM) in Japan

Author

Akanuma Y

Subjects
Adult, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Population, Body Mass Index, Endocrinology, Japan, Risk Factors, Cause of Death, Internal medicine, Diabetes mellitus, Epidemiology, Dietary Carbohydrates, Prevalence, Internal Medicine, Humans, Medicine, Risk factor, education, Cause of death, Glucose tolerance test, education.field_of_study, medicine.diagnostic_test, business.industry, Body Weight, Diabetic retinopathy, Middle Aged, medicine.disease, Dietary Fats, Diet, Diabetes Mellitus, Type 2, Dietary Proteins, Energy Intake, business, Body mass index
Abstract

Before the 1980s, only limited community-based data were available on the prevalence of diabetes in Japan. The prevalence of diabetes in subjects older than 40 years was 2-5%. In many surveys carried out in the 1990s, all subjects were examined using the 75 g glucose tolerance test and diabetes was diagnosed according to the WHO criteria. Diabetes was found in about 10% of the population older than 40 years. A higher prevalence in Japanese immigrants in the United States suggests that change of environmental factors, such as increased intake of animal fat, might further increase the prevalence of diabetes in Japan in the future. The mean BMI of NIDDM patients at their initial visit to our hospital is 22.9 + 3.4 kg m-2, compared to patients in many other developed countries and diabetic Japanese Americans. Regarding causes of death in Japanese diabetic patients, the most frequent causes were vascular diseases including renal failure 11.2%, ischaemic heart diseases 14.6%, and cerebrovascular diseases 13.5%, thus atherosclerotic diseases were less frequent compared to the data in the United States. Each year, approximately 6000 diabetic patients start haemodialysis, and diabetic retinopathy is the main cause of acquired blindness in Japan.

Published
1996

36. The role of PPARγ as a thrifty gene both in mice and humans

Author

Hara, K., primary, Kubota, N., additional, Tobe, K., additional, Terauchi, Y., additional, Miki, H., additional, Komeda, K., additional, Tamemoto, H., additional, Yamauchi, T., additional, Hagura, R., additional, Ito, C., additional, Akanuma, Y., additional, and Kadowaki, T., additional

Published
2000
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37. Disruption of insulin receptor substrate 2 causes type 2 diabetes because of liver insulin resistance and lack of compensatory beta-cell hyperplasia.

Author

Kubota, N, primary, Tobe, K, additional, Terauchi, Y, additional, Eto, K, additional, Yamauchi, T, additional, Suzuki, R, additional, Tsubamoto, Y, additional, Komeda, K, additional, Nakano, R, additional, Miki, H, additional, Satoh, S, additional, Sekihara, H, additional, Sciacchitano, S, additional, Lesniak, M, additional, Aizawa, S, additional, Nagai, R, additional, Kimura, S, additional, Akanuma, Y, additional, Taylor, S I, additional, and Kadowaki, T, additional

Published
2000
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43. Development of non-insulin-dependent diabetes mellitus in the double knockout mice with disruption of insulin receptor substrate-1 and beta cell glucokinase genes. Genetic reconstitution of diabetes as a polygenic disease.

Author

Terauchi, Y, primary, Iwamoto, K, additional, Tamemoto, H, additional, Komeda, K, additional, Ishii, C, additional, Kanazawa, Y, additional, Asanuma, N, additional, Aizawa, T, additional, Akanuma, Y, additional, Yasuda, K, additional, Kodama, T, additional, Tobe, K, additional, Yazaki, Y, additional, and Kadowaki, T, additional

Published
1997
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45. A Mutation in the β3-Adrenergic Receptor Gene Is Associated with Obesity and Hyperinsulinemia in Japanese Subjects

Author

Kadowaki, H., primary, Yasuda, K., additional, Iwamoto, K., additional, Otabe, S., additional, Shimokawa, K., additional, Silver, K., additional, Walston, J., additional, Yoshinaga, H., additional, Kosaka, K., additional, Yamada, N., additional, Saito, Y., additional, Hagura, R., additional, Akanuma, Y., additional, Shuldiner, A., additional, Yazaki, Y., additional, and Kadowaki, T., additional

Published
1995
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